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This Article Full Text Full Text (PDF) All Versions of this Article: ASN.2009020133v1 ASN.2009020133v2 21/1/42    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Eller, K. Articles by Rot, A. PubMed PubMed Citation Articles by Eller, K. Articles by Rot, A. Related Collections Related Article

CCR7 Deficiency Exacerbates Injury in Acute Nephritis Due to Aberrant Localization of Regulatory T Cells

Kathrin Eller^*, Tobias Weber^*, Monika Pruenster, Anna M. Wolf, Gert Mayer^*, Alexander R. Rosenkranz^* and Antal Rot

*Department of Internal Medicine IV–Nephrology and Hypertension and
Tyrolean Cancer Research Institute, Laboratory of Tumor Immunology, Innsbruck Medical University, Innsbruck, Austria;
Walter-Brendel-Center, Ludwig-Maximilian-Universität, Munich, Germany; and
MRC Centre for Immune Regulation, Institute of Biomedical Research, University of Birmingham, Birmingham, United Kingdom

Correspondence: Dr. Alexander R. Rosenkranz, Innsbruck Medical University, Clinical Division of Internal Medicine IV–Nephrology and Hypertension, Anichstrasse. 35, 6020 Innsbruck, Austria. Phone: +43-512-504-81333; Fax: +43-512-504-23309; E-mail: alexander.rosenkranz{at}i-med.ac.at or Dr. Antal Rot, MRC Centre for Immune Regulation, Institute of Biomedical Research, University of Birmingham, Edgebaston, Birmingham, B152TT, UK. Phone: +44-121-414-3454; Fax: +44-121-414-3599; E-mail: a.rot{at}bham.ac.uk

Received for publication February 2, 2009. Accepted for publication September 14, 2009.

The homing of dendritic cells and T cells to secondary lymphoid organs requires chemokine receptor 7 (CCR7) expression on these cells. T cells mediate the pathogenesis of experimental accelerated nephrotoxic serum nephritis (NTS), including its suppression by regulatory T cells (Tregs), but the contribution of CCR7 to this disease is unknown. Here, we compared the development of NTS in CCR7-knockout (KO) and wild-type (WT) mice. Compared with WT mice, CCR7KO mice developed more severe disease with significantly more inflammatory cells infiltrating the kidney. These cells included FoxP3⁺ Tregs, which were virtually absent from WT kidneys. The adoptive transfer of WT Tregs into CCR7KO mice at the time of immunization protected the recipients from disease; these cells homed to secondary lymphoid organs but not to kidneys. Conversely, adoptive transfer of CCR7KO Tregs into WT mice did not inhibit development of NTS. These data suggest that NTS can develop without CCR7 expression, but Treg-mediated disease suppression, which seems to occur in secondary lymphoid organs, requires CCR7.

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				O. M. Steinmetz, J.-E. Turner, and U. Panzer Staying on Top of Things Right from the Start: The Obsessive-Compulsive Disorder of Regulatory T Cells J. Am. Soc. Nephrol., January 1, 2010; 21(1): 6 - 7. [Full Text] [PDF]

Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673