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Published ahead of print on September 5, 2007
J Am Soc Nephrol 18: 2628-2635, 2007
© 2007 American Society of Nephrology
doi: 10.1681/ASN.2007030273
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Brief Reviews

Dendritic Cells in the Kidney

Rohan John{dagger} and Peter J. Nelson{dagger}

{dagger} Division of Nephrology, New York University School of Medicine, New York, New York

Correspondence: Dr. Peter J. Nelson, Division of Nephrology, New York University School of Medicine, Smilow Research Center, 522 First Avenue, New York, NY 10016. Phone: 212-263-7681; Fax: 212-263-7683; E-mail: nelsop02{at}popmail.med.nyu.edu


   Abstract
Top
 Abstract
Introduction
 IDENTIFICATION OF THE RDC...
 ORIGINS AND MIGRATION OF...
 FUNCTION OF RDC
 CONCLUSIONS
 Disclosures
 References
 
Dendritic cells (DC) in nonlymphoid organs function at the crossroads of innate and adaptive immunity, self-tolerance, and tissue homeostasis. This review provides an overview of the study of DC in the kidney, tracing its history leading to the current knowledge of the origins, migration, and function of renal DC. Together, these studies suggest that renal DC play a critical role in the health and disease of the kidney, opening the way to direct targeting of renal DC for therapeutic benefit.


   Introduction
Top
 Abstract
 Introduction
IDENTIFICATION OF THE RDC...
 ORIGINS AND MIGRATION OF...
 FUNCTION OF RDC
 CONCLUSIONS
 Disclosures
 References
 
Dendritic cells (DC) have been extensively studied in lymphoid and many nonlymphoid organs in the past three decades but have received comparatively little attention in the kidney. One reason for this disparity has been an apparent difficulty in identifying, isolating, and manipulating renal DC (rDC) in vitro and in vivo to gain a better understanding of their function in the kidney. These barriers to the study of rDC have fallen in recent years, and it is now clear that rDC exist in intimate communication with the entire renal parenchyma, constantly surveying for and responding to local environmental cues. Here, we review the history of the identification of the rDC network; the origins and migration of rDC at steady state; and the function of rDC in innate and adaptive immunity, self-tolerance, and homeostasis of the renal parenchyma.


   IDENTIFICATION OF THE RDC NETWORK
Top
 Abstract
 Introduction
 IDENTIFICATION OF THE RDC...
ORIGINS AND MIGRATION OF...
 FUNCTION OF RDC
 CONCLUSIONS
 Disclosures
 References
 
Ground-breaking studies in the 1970s by Steinman and colleagues1,2 identified and functionally segregated "dendritic cells" from other immunocytes in lymphoid organs. This led to the discovery that splenic DC potently stimulated the proliferation of T lymphocytes in mixed leukocyte reactions and expressed surface Ia antigens,3 identifying DC as MHC class II+. rDC in rat kidney were subsequently recognized in 1981 by the existence of resident MHC class II+ cells with stellate and "mononuclear phagocyte" morphology in the renal interstitium4,5 and mesangium.6 These anatomic locations were subsequently confirmed by electron microscopy7,8; however, proof that rDC alloactivate T lymphocytes, similar to DC isolated from lymphoid tissues, was not reported until 19949 or substantiated until more recently,10–12 after the ability to isolate rDC via CD11c (the integrin {alpha}x chain) expressed by differentiated mouse DC.13 Similar to other DC, differentiated rDC were also characterized as "immature" versus "mature" on the basis of their low versus high expression of co-stimulatory molecules, respectively.

Several functional subsets of DC have now been phenotyped,13–18 and some of these subsets have been identified in the kidney using defined markers (Table 1). Within normal mouse kidneys, >90 to 95% of CD11c+ rDC are negative for CD8{alpha} and CD45RA (B220),10,12,19 indicating that the majority of mouse rDC are of the myeloid lineage and major constituents of the mononuclear phagocyte system within the kidney.19,20 Small numbers of lymphoid (CD11c+CD8{alpha}+B220–; this subset has been identified in mice but not in humans13) and preplasmacytoid (CD11c+CD8{alpha}–B220+) rDC have also been detected within mouse kidneys.10,19 Within normal human kidneys, myeloid (BDCA-1+DC-SIGN+ and BDCA-1+DC-SIGN–) and preplasmacytoid (BDCA-2+DC-SIGN–) rDC were recently identified, and on the basis of the quantitative area of positive staining for BDCA-1 versus BDCA-2 in thin sections, preplasmacytoid rDC represent a greater fraction of total rDC in normal human kidneys as compared with normal mouse kidneys (up to 20% versus <10%, respectively).10,19,21 Whether mouse or human kidneys harbor or recruit any of the most recently defined functional DC, such as IFN-producing killer DC,22,23 inflammatory TNF-{alpha}/inducible nitric oxide synthase–producing DC,24,25 and tolerogenic IDO-expressing DC,26–31 is unclear.


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  		Table 1. Representative markers of rDC subsets at steady state10–12,19,21

 
Unequivocal evidence that rDC form a true anatomic surveillance network within the renal parenchyma, rather than a random dispersion at steady state, was determined by examination of rDC in situ in the kidneys of CX3CR1GFP/+ mice (Figure 1).19 Under intravital and confocal microscopy from the capsule to the papilla of kidneys in CX3CR1GFP/+ mice, stellate-shaped myeloid rDC form a contiguous network throughout the entire interstitium, encasing all nephrons.19 Confirming previous studies,6,7 myeloid rDC that resemble pre-DC (analogous to the globular shape of resident preplasmacytoid DC15) are also present at low density within the mesangium of CX3CR1GFP/+ mice.19 Importantly, recent studies indicated that a similar anatomic surveillance network of rDC exists throughout the interstitium and mesangium of normal human kidneys.21 Therefore, at steady state, rDC are positioned to respond immediately to "danger" or "tolerogenic" signals32 anywhere within the renal parenchyma, whether derived from self or nonself sources.


Figure 1
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  		Figure 1. Surveillance of the renal parenchyma by the rDC network. The three panels shown are high-power views of the same location in the outer medulla of a normal kidney from a CX3CR1GFP/+ mouse captured by confocal microscopy. The resident rDC network (A) is an anatomically separate cellular compartment from the renal parenchyma that it surveys (B). This affords rDC the ability to respond rapidly to local environmental cues, to migrate apart from nephrons, and to communicate with other components of the immune system both within and outside the kidney. (C) Merge of A and B demonstrates the intimate relationship that exists between rDC and the renal parenchyma.

 

   ORIGINS AND MIGRATION OF RDC AT STEADY STATE
Top
 Abstract
 Introduction
 IDENTIFICATION OF THE RDC...
 ORIGINS AND MIGRATION OF...
FUNCTION OF RDC
 CONCLUSIONS
 Disclosures
 References
 
Similar to DC in other nonlymphoid organs,33–35 rDC constitute a heterogeneous population of bone marrow–derived hematopoietic cells that, unlike DC that function solely within lymphoid tissues (most of the DC in the thymus and spleen and approximately half of the DC in lymph nodes), serve as sentinels within the kidney before trafficking to lymphoid organs.13–18 Because of the plasticity of FLT3+ common myeloid and common lymphoid DC precursors to generate all DC subsets,16 local trophic cues rather than the availability of DC precursors probably determine the constituency of rDC at steady state. Notably, although administration of the ligand for FLT3 to mice can mobilize rDC precursors and transiently increase the total number of rDC, as it does for DC in other tissues,36 the proportion of each rDC subset is not significantly altered when compared with the normal steady state.10

Recent studies of myeloid rDC suggest a probable role of the renal microenvironment in stipulating the heterogeneity of rDC. Deriving from a shared clonogenic progenitor of the mononuclear phagocyte system37 along the long-lived "noninflammatory" CX3CR1highCCR2– monocyte lineage (also Ly6C–GR1– in mice; CD14lowCD16+ in humans),19,38–41 myeloid rDC can express markers conventionally assigned to macrophages (F4/80, CD68).10–12,19,42 This phenotypic overlap between myeloid rDC and macrophages20 is differential within normal kidneys; stellate-shaped CD11c+F4/80+ rDC, for example, predominate in the medulla, whereas globular-shaped MHC class II+ pre-rDC reside in the mesangium.6,7,19,43 This finding suggests that regional inductive factors shape the repertoire of rDC. It is interesting that engagement of the CSF-1 receptor is required for the differentiation and survival of myeloid DC,44 and constitutive expression of CSF-1 (i.e., M-CSF, a major chemoattractant and growth factor for mononuclear phagocytes45) by renal epithelial cells seems to be more prominent in the medulla than in the cortex at steady state.46,47 Whether this alone explains the heterogeneity of rDC is unclear. More likely, other differentially expressed trophic ligands (thymic stromal lymphopoietin-like factors that may be elaborated by renal epithelial cells or interstitial stromal cell populations48,49) and extracellular matrices within the kidney also contribute to the specification of rDC.

Trafficking rDC precursors express several chemokine receptors (CCR)50–53 that are also involved in establishing and maintaining the rDC network. Circulating immature mouse DC mobilized by FLT3 ligand migrate in vitro to CCR ligands expressed at basal levels within normal kidneys and, after adoptive transfer, traffic into the renal interstitium and mesangium in vivo.53 In contrast, isolated immature mouse rDC fail to demonstrate similar migration behavior despite expression of the same CCR.53 This suggests that renal-derived chemokines recruit trafficking rDC precursors at steady state, but once in residence, differentiating rDC precursors undergo CCR desensitization, possibly by molecules other than chemokines.50,53–55 In addition, the lack of redundant cellularity within the contiguous rDC network19 suggests exquisite, reciprocal downregulation or sequestration of chemoattractants directly at sites of occupancy by individual rDC.50

It is intriguing that self-renewal of rDC within the kidney may also occur (analogous to DC in the skin56 and ovaries57), a possibility hinted at by the small population (<3%) of resident CX3CR1highGR1– leukocytes in normal mouse kidneys that lack phenotypic markers of differentiated DC.19 Because preliminary bromodeoxyuridine-labeling experiments in normal mice58 suggest an average half-life across all rDC subsets of approximately 35 d12 (Matthew Griffin, personal communication; Matthew Griffin, MD Associate Professor Mayo Clinic, Rochester, Minnesota, USA, Date of communication: 2/22/07), this latter possibility, if true, will require innovative long-term studies to capture. Approaches such as total body irradiation, long known to be insufficient at fully ablating rDC,59,60 followed by bone marrow transplantation to reform the rDC network does not recapitulate normal rDC homeostasis and can lead to chimerism between donor and recipient rDC56


   FUNCTION OF RDC
Top
 Abstract
 Introduction
 IDENTIFICATION OF THE RDC...
 ORIGINS AND MIGRATION OF...
 FUNCTION OF RDC
CONCLUSIONS
 Disclosures
 References
 
Innate Immunity
As sentinels of the immune system, rDC are positioned to integrate environmental cues and influence innate immune responses anywhere within the kidney.19 This functional plasticity rests in the intrinsic ability of tissue-resident, surveying DC such as immature rDC to sense and sample continually their immediate environment. This surveillance by rDC occurs by multiple mechanisms and includes the following: Engagement of a broad repertoire of surface receptors such as Toll-like receptors,61,62 receptors for alarmins,63 Fc receptors,64,65 complement receptors,65–67 C-type lectin receptors,68–71 scavenger receptors,72,73 and cytokine and CCR; contact or paracrine-mediated signals from trafficking innate immune cells such as neutrophils,74 natural killer cells,75,76 natural killer T lymphocytes,75,77 and {gamma}{delta} T lymphocytes75,78; contact or paracrine-mediated signals from trafficking adaptive immune cells79; and contact (e.g., via tunneling nanotubes19,80) or paracrine-mediated signals from adjacent resident rDC.81

In turn, the rapid integration of these external stimuli by rDC and their subsequent proinflammatory activation (if the stimuli are not tolerogenic) can prime and amplify innate immune responses. This occurs mainly through the secretion of cytokines (e.g., TNF-{alpha}, type I IFN, IL-1beta, IL-2, IL-6, IL-12, IL-15) and chemokines by rDC that act on adjacent renal parenchymal cells and innate immune cells,50,75,82 which includes resident preplasmacytoid DC as "professional type I IFN–producing" leukocytes.15 For example, resident myeloid rDC were recently identified as the predominant source of intrarenal TNF-{alpha} produced during the early "sterile" innate immune response to renal ischemia-reperfusion injury,42 an insult that also induces the maturation and migration of these resident myeloid rDC to lymphoid tissues.12 This initial cytokine response by resident rDC is separate from the cytokines subsequently released by recruited "inflammatory" CX3CR1lowCCR2+ rDC precursors (also Ly6C+GR1+ in mice; CD14hiCD16– in humans).19,38–41 These latter cytokines contribute to sequelae of renal ischemia-reperfusion injury such as interstitial fibrosis,83 analogous to the cytokine response and egress versus influx of rDC12,53,84 versus rDC precursors,85 respectively, in response to LPS.

Adaptive Immunity
Not unexpected, rDC exhibit the hallmarks of well-equipped antigen-presenting cells of the adaptive immune system. Resident rDC at steady state express MHC class I and class II molecules but bear low levels of co-stimulatory molecules (e.g., CD80, CD86, CD40).9–12,19 Resident rDC probe their immediate environment (which may include the lumen of the nephron)19 and capture self and nonself molecules, whether derived from within or outside the kidney, via phagocytosis, pinocytosis, and receptor-mediated endocytosis.12,19 In response to the same "danger" signals that invoke innate immune responses, rDC also upregulate the expression of co-stimulatory molecules and CCR7 (the CCR for ligands, CCL19, and CCL21, expressed by stromal cells in T lymphocyte–rich areas of lymph nodes86,87) and migrate to secondary lymphoid tissues bearing any molecules captured within the kidney (or generated within rDC) for processing and presentation to adaptive immune cells.9,10,12,53

These mature rDC potently stimulate T lymphocyte proliferation9–12 and, depending on the nature of maturing stimuli,61,62,88 presumably secrete cytokines that promote the differentiation of naive T lymphocytes toward specific T helper (Th) effectors such as Th1, Th2, or Th17 lymphocytes89 (this has yet to be formally reported). It is unclear, however, the degree to which environmental cues that are unique to the kidney (e.g., Toll-like receptor recognition of the kidney-restricted protein, Tamm-Horsfall glycoprotein90) "imprint" rDC to polarize preferentially naive T lymphocytes and generate kidney-tropic Th effectors.91 Moreover, little is known regarding environmental cues that may retard the egress of mature, antigen-presenting rDC out of the kidney (as recently shown in the bowel92), a recipe for inducing adaptive immune responses within the kidney itself and subsequently organizing pathogenic "nephron-associated lymphoid tissue."

Self-Tolerance
DC in peripheral tissues contribute to self-tolerance by supplementing central tolerance.93–96 Preliminary studies indicate that rDC also play an important role in maintaining self-tolerance within the kidney. Immature rDC induce the expansion of T regulatory lymphocytes (Treg) in mixed leukocyte reactions and suppress allorecognition in vivo.10 These findings suggest that rDC may be tolerogenic if engaged by T lymphocytes that have escaped thymic selection and are reactive to self-antigens within the kidney. Moreover, cross-presentation of self-antigens derived within the kidney by rDC deletes autoreactive T lymphocytes in vivo by a Fas-mediated mechanism.97–99 These observations are intriguing because several tissue-specific self-antigens demonstrate low or no expression in the thymus and, thus, rely on peripheral mechanisms to help maintain tolerance.100 This is a potential confounder of many experimental kidney-restricted promoter systems that is often ignored. For example, failure to regulate or delete autoreactive T lymphocytes generated during accelerated apoptosis of renal parenchyma, an instigator of autoimmunity,101,102 may explain why CD8+ T lymphocytes directed against kidney antigens, presumably presented by rDC, can develop in kd/kd mice.103,104

The ability of DC to process and present antigen can also be suppressed after contact with Treg,105,106 raising the possibility that resident rDC themselves are targets for trafficking Treg. Notably, Treg ameliorate both the acute and chronic phases of renal disease in disparate models of immune-mediated renal injury,107–109 although rDC–Treg interactions have not been studied in these experiments. This possible interaction is an exciting area of future inquiry, as is the potential to manipulate the reciprocal relationship between rDC and Treg to suppress immune responses that may be coordinated by rDC.110

Immunologic Homeostasis of the Renal Parenchyma
Surveillance by DC resident in tissues may mediate self-tolerance to and regeneration of dying parenchymal cells.102,111,112 There is mounting evidence that the rDC network may fulfill this crucial role within the kidney. In mice, "alternatively" activated mononuclear phagocytes (i.e., an anti-inflammatory tolerogenic state in contrast to the "classically" activated proinflammatory state113) clear apoptotic cells within the developing kidney as early as embryonic day 12, and challenge of embryonic kidney explants with M-CSF rapidly accelerates ureteric branching and nephron induction114 (David Hume, personal communication; David Hume, PhD Professor University of Queensland, Brisbane, Australia, Date of communication: 2/20/07). This suggests the establishment of mechanisms of apoptotic clearance during nephrogenesis that are coupled to paracrine growth loops115,116 between rDC and the renal parenchyma that persist in the mature kidney. It is interesting that hepatocyte growth factor, an important growth factor for renal epithelial cells,117 also alternatively activates DC,118 and DC that are matured in the presence of anti-inflammatory factors selectively express angiogenic isoforms of vascular endothelial growth factor.119 Although preliminary, these studies collectively suggest that rDC may participate in a coordinated program to control growth and maintain the homeostatic function of the renal parenchyma.


   CONCLUSIONS
Top
 Abstract
 Introduction
 IDENTIFICATION OF THE RDC...
 ORIGINS AND MIGRATION OF...
 FUNCTION OF RDC
 CONCLUSIONS
Disclosures
 References
 
In this brief review, we have discussed the current knowledge surrounding rDC. rDC function in the fundamental immunologic paradigm of continual surveillance. This is evidenced by the anatomic availability and intrinsic ability of rDC to respond rapidly to environmental cues anywhere within the kidney. rDC migrate and communicate these cues to both arms of the immune system and to the renal parenchyma and renew to maintain a contiguous network. In many respects, our understanding of rDC in the health and disease of the kidney is very rudimentary, spawned in part by the considerable lag in research on rDC compared with DC in other organs and tissues. Fortuitously, much is now known about the biology of DC in general. Application of this knowledge should yield rapid and important advances in deciphering the contribution of rDC to the pathogenesis, such as their role in HIV infection in the kidney,120,121 and treatment, such as their targeting by CDK/GSK-3 inhibitors,122,123 of many renal diseases. This inquiry promises to be revealing in the years immediately ahead.


   Disclosures
Top
 Abstract
 Introduction
 IDENTIFICATION OF THE RDC...
 ORIGINS AND MIGRATION OF...
 FUNCTION OF RDC
 CONCLUSIONS
 Disclosures
References
 
None.


   Acknowledgments
 
P.J.N. is supported by National Institutes of Health grants DK065498 and DK079498.

We thank Matthew Griffin for critical reading of the manuscript and David Hume for helpful discussions on the role of mononuclear phagocytes in nephrogenesis. Rohan John was a visiting fellow at the NYU School of Medicine.


   Footnotes
 
Published online ahead of print. Publication date available at www.jasn.org.


   References
Top
 Abstract
 Introduction
 IDENTIFICATION OF THE RDC...
 ORIGINS AND MIGRATION OF...
 FUNCTION OF RDC
 CONCLUSIONS
 Disclosures
 References
 

  1. Steinman RM, Witmer MD: Lymphoid dendritic cells are potent stimulators of the primary mixed leukocyte reaction in mice. Proc Natl Acad Sci U S A 75 : 5132 –5136, 1978[Abstract/Free Full Text]
  2. Nussenzweig MC, Steinman RM: Contribution of dendritic cells to stimulation of the murine syngeneic mixed leukocyte reaction. J Exp Med 151 : 1196 –1212, 1980[Abstract/Free Full Text]
  3. Steinman RM, Kaplan G, Witmer MD, Cohn ZA: Identification of a novel cell type in peripheral lymphoid organs of mice. V. Purification of spleen dendritic cells, new surface markers, and maintenance in vitro. J Exp Med 149 : 1 –16, 1979[Abstract/Free Full Text]
  4. Hart DN, Fabre JW: Demonstration and characterization of Ia-positive dendritic cells in the interstitial connective tissues of rat heart and other tissues, but not brain. J Exp Med 154 : 347 –361, 1981[Abstract/Free Full Text]
  5. Hart DN, Fabre JW: Major histocompatibility complex antigens in rat kidney, ureter, and bladder. Localization with monoclonal antibodies and demonstration of Ia-positive dendritic cells. Transplantation 31 : 318 –325, 1981[Medline]
  6. Schreiner GF, Kiely JM, Cotran RS, Unanue ER: Characterization of resident glomerular cells in the rat expressing Ia determinants and manifesting genetically restricted interactions with lymphocytes. J Clin Invest 68 : 920 –931, 1981[Medline]
  7. Schreiner GF, Cotran RS: Localization of an Ia-bearing glomerular cell in the mesangium. J Cell Biol 94 : 483 –488, 1982[Abstract/Free Full Text]
  8. Kaissling B, Le Hir M: Characterization and distribution of interstitial cell types in the renal cortex of rats. Kidney Int 45 : 709 –720, 1994[Medline]
  9. Austyn JM, Hankins DF, Larsen CP, Morris PJ, Rao AS, Roake JA: Isolation and characterization of dendritic cells from mouse heart and kidney. J Immunol 152 : 2401 –2410, 1994[Abstract]
  10. Coates PT, Duncan FJ, Colvin BL, Wang Z, Zahorchak AF, Shufesky WJ, Morelli AE, Thomson AW: In vivo-mobilized kidney dendritic cells are functionally immature, subvert alloreactive T-cell responses, and prolong organ allograft survival. Transplantation 77 : 1080 –1089, 2004[CrossRef][Medline]
  11. Kruger T, Benke D, Eitner F, Lang A, Wirtz M, Hamilton-Williams EE, Engel D, Giese B, Muller-Newen G, Floege J, Kurts C: Identification and functional characterization of dendritic cells in the healthy murine kidney and in experimental glomerulonephritis. J Am Soc Nephrol 15 : 613 –621, 2004[Abstract/Free Full Text]
  12. Dong X, Swaminathan S, Bachman LA, Croatt AJ, Nath KA, Griffin MD: Antigen presentation by dendritic cells in renal lymph nodes is linked to systemic and local injury to the kidney. Kidney Int 68 : 1096 –1108, 2005[CrossRef][Medline]
  13. Shortman K, Liu YJ: Mouse and human dendritic cell subtypes. Nat Rev Immunol 2 : 151 –161, 2002[CrossRef][Medline]
  14. Ardavin C: Origin, precursors and differentiation of mouse dendritic cells. Nat Rev Immunol 3 : 582 –590, 2003[CrossRef][Medline]
  15. Soumelis V, Liu YJ: From plasmacytoid to dendritic cell: Morphological and functional switches during plasmacytoid pre-dendritic cell differentiation. Eur J Immunol 36 : 2286 –2292, 2006[CrossRef][Medline]
  16. Shortman K, Naik SH: Steady-state and inflammatory dendritic-cell development. Nat Rev Immunol 7 : 19 –30, 2007[CrossRef][Medline]
  17. Ito T, Liu YJ, Kadowaki N: Functional diversity and plasticity of human dendritic cell subsets. Int J Hematol 81 : 188 –196, 2005[CrossRef][Medline]
  18. Bonasio R, von Andrian UH: Generation, migration and function of circulating dendritic cells. Curr Opin Immunol 18 : 503 –511, 2006[CrossRef][Medline]
  19. Soos TJ, Sims TN, Barisoni L, Lin K, Littman DR, Dustin ML, Nelson PJ: CX3CR1+ interstitial dendritic cells form a contiguous network throughout the entire kidney. Kidney Int 70 : 591 –596, 2006[Medline]
  20. Hume DA: The mononuclear phagocyte system. Curr Opin Immunol 18 : 49 –53, 2006[CrossRef][Medline]
  21. Woltman A, de Fijter J, Zuidwijk K, Vlug A, Bajema I, van der Kooij S, van Ham V, van Kooten C: Quantitation of dendritic cell subsets in human renal tissues under normal and pathologic conditions. Kidney Int 71 : 1001 –1008, 2007[CrossRef][Medline]
  22. Chan CW, Crafton E, Fan HN, Flook J, Yoshimura K, Skarica M, Brockstedt D, Dubensky TW, Stins MF, Lanier LL, Pardoll DM, Housseau F: Interferon-producing killer dendritic cells provide a link between innate and adaptive immunity. Nat Med 12 : 207 –213, 2006[CrossRef][Medline]
  23. Taieb J, Chaput N, Menard C, Apetoh L, Ullrich E, Bonmort M, Pequignot M, Casares N, Terme M, Flament C, Opolon P, Lecluse Y, Metivier D, Tomasello E, Vivier E, Ghiringhelli F, Martin F, Klatzmann D, Poynard T, Tursz T, Raposo G, Yagita H, Ryffel B, Kroemer G, Zitvogel L: A novel dendritic cell subset involved in tumor immunosurveillance. Nat Med 12 : 214 –219, 2006[CrossRef][Medline]
  24. Serbina NV, Salazar-Mather TP, Biron CA, Kuziel WA, Pamer EG: TNF/iNOS-producing dendritic cells mediate innate immune defense against bacterial infection. Immunity 19 : 59 –70, 2003[CrossRef][Medline]
  25. Engel D, Dobrindt U, Tittel A, Peters P, Maurer J, Gutgemann I, Kaissling B, Kuziel W, Jung S, Kurts C: Tumor necrosis factor alpha- and inducible nitric oxide synthase-producing dendritic cells are rapidly recruited to the bladder in urinary tract infection but are dispensable for bacterial clearance. Infect Immun 74 : 6100 –6107, 2006[Abstract/Free Full Text]
  26. Munn DH, Sharma MD, Lee JR, Jhaver KG, Johnson TS, Keskin DB, Marshall B, Chandler P, Antonia SJ, Burgess R, Slingluff CL Jr, Mellor AL: Potential regulatory function of human dendritic cells expressing indoleamine 2,3-dioxygenase. Science 297 : 1867 –1870, 2002[Abstract/Free Full Text]
  27. Baban B, Hansen AM, Chandler PR, Manlapat A, Bingaman A, Kahler DJ, Munn DH, Mellor AL: A minor population of splenic dendritic cells expressing CD19 mediates IDO-dependent T cell suppression via type I IFN signaling following B7 ligation. Int Immunol 17 : 909 –919, 2005[Abstract/Free Full Text]
  28. Mellor AL, Baban B, Chandler PR, Manlapat A, Kahler DJ, Munn DH: Cutting edge: CpG oligonucleotides induce splenic CD19+ dendritic cells to acquire potent indoleamine 2,3-dioxygenase-dependent T cell regulatory functions via IFN type 1 signaling. J Immunol 175 : 5601 –5605, 2005[Abstract/Free Full Text]
  29. Fallarino F, Grohmann U, Hwang KW, Orabona C, Vacca C, Bianchi R, Belladonna ML, Fioretti MC, Alegre ML, Puccetti P: Modulation of tryptophan catabolism by regulatory T cells. Nat Immunol 4 : 1206 –1212, 2003[CrossRef][Medline]
  30. Mellor AL, Baban B, Chandler P, Marshall B, Jhaver K, Hansen A, Koni PA, Iwashima M, Munn DH: Cutting edge: induced indoleamine 2,3 dioxygenase expression in dendritic cell subsets suppresses T cell clonal expansion. J Immunol 171 : 1652 –1655, 2003[Abstract/Free Full Text]
  31. Munn DH, Sharma MD, Hou D, Baban B, Lee JR, Antonia SJ, Messina JL, Chandler P, Koni PA, Mellor AL: Expression of indoleamine 2,3-dioxygenase by plasmacytoid dendritic cells in tumor-draining lymph nodes. J Clin Invest 114 : 280 –290, 2004[CrossRef][Medline]
  32. Matzinger P: Tolerance, danger, and the extended family. Annu Rev Immunol 12 : 991 –1045, 1994[Medline]
  33. Pillarisetty VG, Shah AB, Miller G, Bleier JI, DeMatteo RP: Liver dendritic cells are less immunogenic than spleen dendritic cells because of differences in subtype composition. J Immunol 172 : 1009 –1017, 2004[Abstract/Free Full Text]
  34. von Garnier C, Filgueira L, Wikstrom M, Smith M, Thomas JA, Strickland DH, Holt PG, Stumbles PA: Anatomical location determines the distribution and function of dendritic cells and other APCs in the respiratory tract. J Immunol 175 : 1609 –1618, 2005[Abstract/Free Full Text]
  35. Masten BJ, Olson GK, Tarleton CA, Rund C, Schuyler M, Mehran R, Archibeque T, Lipscomb MF: Characterization of myeloid and plasmacytoid dendritic cells in human lung. J Immunol 177 : 7784 –7793, 2006[Abstract/Free Full Text]
  36. Maraskovsky E, Brasel K, Teepe M, Roux ER, Lyman SD, Shortman K, McKenna HJ: Dramatic increase in the numbers of functionally mature dendritic cells in Flt3 ligand-treated mice: Multiple dendritic cell subpopulations identified. J Exp Med 184 : 1953 –1962, 1996[Abstract/Free Full Text]
  37. Fogg DK, Sibon C, Miled C, Jung S, Aucouturier P, Littman DR, Cumano A, Geissmann F: A clonogenic bone marrow progenitor specific for macrophages and dendritic cells. Science 311 : 83 –87, 2006[Abstract/Free Full Text]
  38. Geissmann F, Jung S, Littman DR: Blood monocytes consist of two principal subsets with distinct migratory properties. Immunity 19 : 71 –82, 2003[CrossRef][Medline]
  39. Sunderkotter C, Nikolic T, Dillon MJ, Van Rooijen N, Stehling M, Drevets DA, Leenen PJ: Subpopulations of mouse blood monocytes differ in maturation stage and inflammatory response. J Immunol 172 : 4410 –4417, 2004[Abstract/Free Full Text]
  40. Gordon S, Taylor PR: Monocyte and macrophage heterogeneity. Nat Rev Immunol 5 : 953 –964, 2005[CrossRef][Medline]
  41. Yrlid U, Jenkins CD, MacPherson GG: Relationships between distinct blood monocyte subsets and migrating intestinal lymph dendritic cells in vivo under steady-state conditions. J Immunol 176 : 4155 –4162, 2006[Abstract/Free Full Text]
  42. Dong X, Swaminathan S, Bachman LA, Croatt AJ, Nath KA, Griffin MD: Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemia-reperfusion injury. Kidney Int 71 : 619 –628, 2007[CrossRef][Medline]
  43. Hume DA, Gordon S: Mononuclear phagocyte system of the mouse defined by immunohistochemical localization of antigen F4/80. Identification of resident macrophages in renal medullary and cortical interstitium and the juxtaglomerular complex. J Exp Med 157 : 1704 –1709, 1983[Abstract/Free Full Text]
  44. MacDonald KP, Rowe V, Bofinger HM, Thomas R, Sasmono T, Hume DA, Hill GR: The colony-stimulating factor 1 receptor is expressed on dendritic cells during differentiation and regulates their expansion. J Immunol 175 : 1399 –1405, 2005[Abstract/Free Full Text]
  45. Chitu V, Stanley ER: Colony-stimulating factor-1 in immunity and inflammation. Curr Opin Immunol 18 : 39 –48, 2006[CrossRef][Medline]
  46. Isbel NM, Hill PA, Foti R, Mu W, Hurst LA, Stambe C, Lan HY, Atkins RC, Nikolic-Paterson DJ: Tubules are the major site of M-CSF production in experimental kidney disease: Correlation with local macrophage proliferation. Kidney Int 60 : 614 –625, 2001[CrossRef][Medline]
  47. Jang MH, Herber DM, Jiang X, Nandi S, Dai XM, Zeller G, Stanley ER, Kelley VR: Distinct in vivo roles of colony-stimulating factor-1 isoforms in renal inflammation. J Immunol 177 : 4055 –4063, 2006[Abstract/Free Full Text]
  48. Liu YJ, Soumelis V, Watanabe N, Ito T, Wang YH, Malefyt RD, Omori M, Zhou B, Ziegler SF: TSLP: An epithelial cell cytokine that regulates T cell differentiation by conditioning dendritic cell maturation. Annu Rev Immunol 25 : 193 –219, 2007[CrossRef][Medline]
  49. Svensson M, Kaye PM: Stromal-cell regulation of dendritic-cell differentiation and function. Trends Immunol 27 : 580 –587, 2006[CrossRef][Medline]
  50. Sozzani S: Dendritic cell trafficking: more than just chemokines. Cytokine Growth Factor Rev 16 : 581 –592, 2005[CrossRef][Medline]
  51. McColl SR: Chemokines and dendritic cells: A crucial alliance. Immunol Cell Biol 80 : 489 –496, 2002[CrossRef][Medline]
  52. Cavanagh LL, Von Andrian UH: Travellers in many guises: The origins and destinations of dendritic cells. Immunol Cell Biol 80 : 448 –462, 2002[CrossRef][Medline]
  53. Coates PT, Colvin BL, Ranganathan A, Duncan FJ, Lan YY, Shufesky WJ, Zahorchak AF, Morelli AE, Thomson AW: CCR and CC chemokine expression in relation to Flt3 ligand-induced renal dendritic cell mobilization. Kidney Int 66 : 1907 –1917, 2004[CrossRef][Medline]
  54. Vecchi A, Massimiliano L, Ramponi S, Luini W, Bernasconi S, Bonecchi R, Allavena P, Parmentier M, Mantovani A, Sozzani S: Differential responsiveness to constitutive vs. inducible chemokines of immature and mature mouse dendritic cells. J Leukoc Biol 66 : 489 –494, 1999[Abstract]
  55. Le Y, Wetzel MA, Shen W, Gong W, Rogers TJ, Henderson EE, Wang JM: Desensitization of chemokine receptor CCR5 in dendritic cells at the early stage of differentiation by activation of formyl peptide receptors. Clin Immunol 99 : 365 –372, 2001[CrossRef][Medline]
  56. Merad M, Manz MG, Karsunky H, Wagers A, Peters W, Charo I, Weissman IL, Cyster JG, Engleman EG: Langerhans cells renew in the skin throughout life under steady-state conditions. Nat Immunol 3 : 1135 –1141, 2002[CrossRef][Medline]
  57. Pascual CJ, Sanberg PR, Chamizo W, Haraguchi S, Lerner D, Baldwin M, El-Badri NS: Ovarian monocyte progenitor cells: phenotypic and functional characterization. Stem Cells Dev 14 : 173 –180, 2005[CrossRef][Medline]
  58. Kamath AT, Henri S, Battye F, Tough DF, Shortman K: Developmental kinetics and lifespan of dendritic cells in mouse lymphoid organs. Blood 100 : 1734 –1741, 2002[Abstract/Free Full Text]
  59. McKenzie JL, Beard ME, Hart DN: Depletion of donor kidney dendritic cells prolongs graft survival. Transplant Proc 16 : 948 –951, 1984[Medline]
  60. Stein-Oakley AN, Jablonski P, Kraft N, Biguzas M, Howard BO, Marshall VC, Thomson NM: Differential irradiation effects on rat interstitial dendritic cells. Transplant Proc 23 : 632 –634, 1991[Medline]
  61. Iwasaki A, Medzhitov R: Toll-like receptor control of the adaptive immune responses. Nat Immunol 5 : 987 –995, 2004[CrossRef][Medline]
  62. Mazzoni A, Segal DM: Controlling the Toll road to dendritic cell polarization. J Leukoc Biol 75 : 721 –730, 2004[Abstract/Free Full Text]
  63. Oppenheim JJ, Yang D: Alarmins: Chemotactic activators of immune responses. Curr Opin Immunol 17 : 359 –365, 2005[CrossRef][Medline]
  64. Nimmerjahn F, Ravetch JV: Fcgamma receptors: Old friends and new family members. Immunity 24 : 19 –28, 2006[CrossRef][Medline]
  65. Bajtay Z, Csomor E, Sandor N, Erdei A: Expression and role of Fc- and complement-receptors on human dendritic cells. Immunol Lett 104 : 46 –52, 2006[CrossRef][Medline]
  66. Kohl J: The role of complement in danger sensing and transmission. Immunol Res 34 : 157 –176, 2006[CrossRef][Medline]
  67. Zhou W, Peng Q, Li K, Sacks SH: Role of dendritic cell synthesis of complement in the allospecific T cell response. Mol Immunol 44 : 57 –63, 2007[CrossRef][Medline]
  68. Apostolopoulos V, McKenzie IF: Role of the mannose receptor in the immune response. Curr Mol Med 1 : 469 –474, 2001[CrossRef][Medline]
  69. Allavena P, Chieppa M, Monti P, Piemonti L: From pattern recognition receptor to regulator of homeostasis: the double-faced macrophage mannose receptor. Crit Rev Immunol 24 : 179 –192, 2004[CrossRef][Medline]
  70. Gijzen K, Cambi A, Torensma R, Figdor CG: C-type lectins on dendritic cells and their interaction with pathogen-derived and endogenous glycoconjugates. Curr Protein Pept Sci 7 : 283 –294, 2006[CrossRef][Medline]
  71. Kanazawa N: Dendritic cell immunoreceptors: C-type lectin receptors for pattern-recognition and signaling on antigen-presenting cells. J Dermatol Sci 45 : 77 –86, 2007[CrossRef][Medline]
  72. Peiser L, Mukhopadhyay S, Gordon S: Scavenger receptors in innate immunity. Curr Opin Immunol 14 : 123 –128, 2002[CrossRef][Medline]
  73. Becker M, Cotena A, Gordon S, Platt N: Expression of the class A macrophage scavenger receptor on specific subpopulations of murine dendritic cells limits their endotoxin response. Eur J Immunol 36 : 950 –960, 2006[CrossRef][Medline]
  74. Ludwig IS, Geijtenbeek TB, van Kooyk Y: Two way communication between neutrophils and dendritic cells. Curr Opin Pharmacol 6 : 408 –413, 2006[CrossRef][Medline]
  75. Munz C, Steinman RM, Fujii S: Dendritic cell maturation by innate lymphocytes: Coordinated stimulation of innate and adaptive immunity. J Exp Med 202 : 203 –207, 2005[Abstract/Free Full Text]
  76. Walzer T, Dalod M, Vivier E, Zitvogel L: Natural killer cell-dendritic cell crosstalk in the initiation of immune responses. Expert Opin Biol Ther 5[Suppl 1] : S49 –S59, 2005
  77. Montoya CJ, Jie HB, Al-Harthi L, Mulder C, Patino PJ, Rugeles MT, Krieg AM, Landay AL, Wilson SB: Activation of plasmacytoid dendritic cells with TLR9 agonists initiates invariant NKT cell-mediated cross-talk with myeloid dendritic cells. J Immunol 177 : 1028 –1039, 2006[Abstract/Free Full Text]
  78. Born WK, Reardon CL, O’Brien RL: The function of gammadelta T cells in innate immunity. Curr Opin Immunol 18 : 31 –38, 2006[CrossRef][Medline]
  79. So T, Lee SW, Croft M: Tumor necrosis factor/tumor necrosis factor receptor family members that positively regulate immunity. Int J Hematol 83 : 1 –11, 2006[CrossRef][Medline]
  80. Watkins SC, Salter RD: Functional connectivity between immune cells mediated by tunneling nanotubules. Immunity 23 : 309 –318, 2005[CrossRef][Medline]
  81. Fonteneau JF, Larsson M, Beignon AS, McKenna K, Dasilva I, Amara A, Liu YJ, Lifson JD, Littman DR, Bhardwaj N: Human immunodeficiency virus type 1 activates plasmacytoid dendritic cells and concomitantly induces the bystander maturation of myeloid dendritic cells. J Virol 78 : 5223 –5232, 2004[Abstract/Free Full Text]
  82. Foti M, Granucci F, Ricciardi-Castagnoli P: A central role for tissue-resident dendritic cells in innate responses. Trends Immunol 25 : 650 –654, 2004[CrossRef][Medline]
  83. Furuichi K, Gao JL, Murphy PM: Chemokine receptor CX3CR1 regulates renal interstitial fibrosis after ischemia-reperfusion injury. Am J Pathol 169 : 372 –387, 2006[Abstract/Free Full Text]
  84. Roake JA, Rao AS, Morris PJ, Larsen CP, Hankins DF, Austyn JM: Dendritic cell loss from nonlymphoid tissues after systemic administration of lipopolysaccharide, tumor necrosis factor, and interleukin 1. J Exp Med 181 : 2237 –2247, 1995[Abstract/Free Full Text]
  85. Roake JA, Rao AS, Morris PJ, Larsen CP, Hankins DF, Austyn JM: Systemic lipopolysaccharide recruits dendritic cell progenitors to nonlymphoid tissues. Transplantation 59 : 1319 –1324, 1995[Medline]
  86. Sanchez-Sanchez N, Riol-Blanco L, Rodriguez-Fernandez JL: The multiple personalities of the chemokine receptor CCR7 in dendritic cells. J Immunol 176 : 5153 –5159, 2006[Abstract/Free Full Text]
  87. Ziegler E, Gueler F, Rong S, Mengel M, Witzke O, Kribben A, Haller H, Kunzendorf U, Krautwald S: CCL19-IgG prevents allograft rejection by impairment of immune cell trafficking. J Am Soc Nephrol 17 : 2521 –2532, 2006[Abstract/Free Full Text]
  88. Vieira PL, de Jong EC, Wierenga EA, Kapsenberg ML, Kalinski P: Development of Th1-inducing capacity in myeloid dendritic cells requires environmental instruction. J Immunol 164 : 4507 –4512, 2000[Abstract/Free Full Text]
  89. Weaver CT, Hatton RD, Mangan PR, Harrington LE: IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu Rev Immunol 25 : 821 –852, 2007[CrossRef][Medline]
  90. Saemann MD, Weichhart T, Zeyda M, Staffler G, Schunn M, Stuhlmeier KM, Sobanov Y, Stulnig TM, Akira S, von Gabain A, von Ahsen U, Horl WH, Zlabinger GJ: Tamm-Horsfall glycoprotein links innate immune cell activation with adaptive immunity via a Toll-like receptor-4-dependent mechanism. J Clin Invest 115 : 468 –475, 2005[CrossRef][Medline]
  91. Agace WW: Tissue-tropic effector T cells: Generation and targeting opportunities. Nat Rev Immunol 6 : 682 –692, 2006[CrossRef][Medline]
  92. Middel P, Raddatz D, Gunawan B, Haller F, Radzun HJ: Increased number of mature dendritic cells in Crohn's disease: Evidence for a chemokine mediated retention mechanism. Gut 55 : 220 –227, 2006[Abstract/Free Full Text]
  93. Steinman RM, Hawiger D, Nussenzweig MC: Tolerogenic dendritic cells. Annu Rev Immunol 21 : 685 –711, 2003[CrossRef][Medline]
  94. Redmond WL, Sherman LA: Peripheral tolerance of CD8 T lymphocytes. Immunity 22 : 275 –284, 2005[CrossRef][Medline]
  95. Gallegos AM, Bevan MJ: Central tolerance: Good but imperfect. Immunol Rev 209 : 290 –296, 2006[CrossRef][Medline]
  96. Bonasio R, Scimone ML, Schaerli P, Grabie N, Lichtman AH, von Andrian UH: Clonal deletion of thymocytes by circulating dendritic cells homing to the thymus. Nat Immunol 7 : 1092 –1100, 2006[CrossRef][Medline]
  97. Kurts C, Heath WR, Kosaka H, Miller JF, Carbone FR: The peripheral deletion of autoreactive CD8+ T cells induced by cross-presentation of self-antigens involves signaling through CD95 (Fas, Apo-1). J Exp Med 188 : 415 –420, 1998[Abstract/Free Full Text]
  98. Kurts C, Kosaka H, Carbone FR, Miller JF, Heath WR: Class I-restricted cross-presentation of exogenous self-antigens leads to deletion of autoreactive CD8(+) T cells. J Exp Med 186 : 239 –245, 1997[Abstract/Free Full Text]
  99. Ackerman AL, Cresswell P: Cellular mechanisms governing cross-presentation of exogenous antigens. Nat Immunol 5 : 678 –684, 2004[CrossRef][Medline]
  100. Kyewski B, Derbinski J: Self-representation in the thymus: An extended view. Nat Rev Immunol 4 : 688 –698, 2004[CrossRef][Medline]
  101. Savill J, Dransfield I, Gregory C, Haslett C: A blast from the past: Clearance of apoptotic cells regulates immune responses. Nat Rev Immunol 2 : 965 –975, 2002[CrossRef][Medline]
  102. Mahoney JA, Rosen A: Apoptosis and autoimmunity. Curr Opin Immunol 17 : 583 –588, 2005[CrossRef][Medline]
  103. Kelly CJ, Korngold R, Mann R, Clayman M, Haverty T, Neilson EG: Spontaneous interstitial nephritis in kdkd mice. II. Characterization of a tubular antigen-specific, H-2K-restricted Lyt-2+ effector T cell that mediates destructive tubulointerstitial injury. J Immunol 136 : 526 –531, 1986[Abstract]
  104. Hancock WW, Tsai TL, Madaio MP, Gasser DL: Cutting edge: Multiple autoimmune pathways in kd/kd mice. J Immunol 171 : 2778 –2781, 2003[Abstract/Free Full Text]
  105. Tang Q, Adams JY, Tooley AJ, Bi M, Fife BT, Serra P, Santamaria P, Locksley RM, Krummel MF, Bluestone JA: Visualizing regulatory T cell control of autoimmune responses in nonobese diabetic mice. Nat Immunol 7 : 83 –92, 2006[CrossRef][Medline]
  106. Tadokoro CE, Shakhar G, Shen S, Ding Y, Lino AC, Maraver A, Lafaille JJ, Dustin ML: Regulatory T cells inhibit stable contacts between CD4+ T cells and dendritic cells in vivo. J Exp Med 203 : 505 –511, 2006[Abstract/Free Full Text]
  107. Wolf D, Hochegger K, Wolf AM, Rumpold HF, Gastl G, Tilg H, Mayer G, Gunsilius E, Rosenkranz AR: CD4+CD25+ regulatory T cells inhibit experimental anti-glomerular basement membrane glomerulonephritis in mice. J Am Soc Nephrol 16 : 1360 –1370, 2005[Abstract/Free Full Text]
  108. Wang YM, Zhang GY, Wang Y, Hu M, Wu H, Watson D, Hori S, Alexander IE, Harris DC, Alexander SI: Foxp3-transduced polyclonal regulatory T cells protect against chronic renal injury from adriamycin. J Am Soc Nephrol 17 : 697 –706, 2006[Abstract/Free Full Text]
  109. Mahajan D, Wang Y, Qin X, Wang Y, Zheng G, Wang YM, Alexander SI, Harris DC: CD4+CD25+ regulatory T cells protect against injury in an innate murine model of chronic kidney disease. J Am Soc Nephrol 17 : 2731 –2741, 2006[Abstract/Free Full Text]
  110. Yamazaki S, Inaba K, Tarbell KV, Steinman RM: Dendritic cells expand antigen-specific Foxp3+ CD25+ CD4+ regulatory T cells including suppressors of alloreactivity. Immunol Rev 212 : 314 –329, 2006[CrossRef][Medline]
  111. Henson PM, Hume DA: Apoptotic cell removal in development and tissue homeostasis. Trends Immunol 27 : 244 –250, 2006[CrossRef][Medline]
  112. Xu W, Roos A, Daha MR, van Kooten C: Dendritic cell and macrophage subsets in the handling of dying cells. Immunobiology 211 : 567 –575, 2006[CrossRef][Medline]
  113. Goerdt S, Orfanos CE: Other functions, other genes: Alternative activation of antigen-presenting cells. Immunity 10 : 137 –142, 1999[CrossRef][Medline]
  114. Little MH, Woods K, Rae F, Campanale N, Taylor D, Ovchinnikov D, Ricardo S, Grimmond DA, Hume DA: Resident renal macrophages play a proliferative role in kidney development [Abstract]. J Am Soc Nephrol 17 : 332A , 2006
  115. Wyckoff J, Wang W, Lin EY, Wang Y, Pixley F, Stanley ER, Graf T, Pollard JW, Segall J, Condeelis J: A paracrine loop between tumor cells and macrophages is required for tumor cell migration in mammary tumors. Cancer Res 64 : 7022 –7029, 2004[Abstract/Free Full Text]
  116. Aharinejad S, Paulus P, Sioud M, Hofmann M, Zins K, Schafer R, Stanley ER, Abraham D: Colony-stimulating factor-1 blockade by antisense oligonucleotides and small interfering RNAs suppresses growth of human mammary tumor xenografts in mice. Cancer Res 64 : 5378 –5384, 2004[Abstract/Free Full Text]
  117. Liu Y: Hepatocyte growth factor and the kidney. Curr Opin Nephrol Hypertens 11 : 23 –30, 2002[CrossRef][Medline]
  118. Okunishi K, Dohi M, Nakagome K, Tanaka R, Mizuno S, Matsumoto K, Miyazaki J, Nakamura T, Yamamoto K: A novel role of hepatocyte growth factor as an immune regulator through suppressing dendritic cell function. J Immunol 175 : 4745 –4753, 2005[Abstract/Free Full Text]
  119. Riboldi E, Musso T, Moroni E, Urbinati C, Bernasconi S, Rusnati M, Adorini L, Presta M, Sozzani S: Cutting edge: Proangiogenic properties of alternatively activated dendritic cells. J Immunol 175 : 2788 –2792, 2005[Abstract/Free Full Text]
  120. Larsson M: HIV-1 and the hijacking of dendritic cells: A tug of war. Springer Semin Immun 26 : 309 –328, 2005[CrossRef]
  121. Wu L, KewalRamani VN: Dendritic-cell interactions with HIV: Infection and viral dissemination. Nat Rev Immunol 6 : 859 –868, 2006[CrossRef][Medline]
  122. Martin M, Rehani K, Jope RS, Michalek SM: Toll-like receptor-mediated cytokine production is differentially regulated by glycogen synthase kinase 3. Nat Immunol 6 : 777 –784, 2005[CrossRef][Medline]
  123. Soos TJ, Meijer L, Nelson PJ: CDK/GSK-3 inhibitors as a new approach for the treatment of proliferative renal diseases. Drug News Perspect 19 : 325 –328, 2006[CrossRef][Medline]



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