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Published ahead of print on October 5, 2005
J Am Soc Nephrol 16: 3572-3582, 2005
© 2005 American Society of Nephrology
doi: 10.1681/ASN.2005040373
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Basic Immunology and Pathology

C5a Receptor Deficiency Attenuates T Cell Function and Renal Disease in MRLlpr Mice

Scott E. Wenderfer*,{dagger}, Baozhen Ke*, Travis J. Hollmann*, Rick A. Wetsel*, Hui Yao Lan{ddagger} and Michael C. Braun*,{dagger}

* Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases and {dagger} Division of Pediatric Nephrology and Hypertension, Department of Pediatrics, University of Texas Health Science Center–Houston, Houston, Texas; and {ddagger} Section of Nephrology, Department of Internal Medicine, Baylor College of Medicine, Houston, Texas

Address correspondence to: Dr. Michael C. Braun, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center, 2121 W. Holcombe Blvd., Houston, TX 77030. Phone: 713-500-2438; Fax: 713-500-2424; E-mail: michael.c.braun{at}uth.tmc.edu

Received for publication April 8, 2005. Accepted for publication August 13, 2005.

The development and progression of systemic lupus erythematosus (SLE) is strongly associated with complement activation and deposition. To characterize the role of C5a and its receptor (C5aR) in SLE, C5aR-deficient mice were backcrossed nine generations onto the lupus-like MRLlpr genetic background. Evidence is presented that C5aR modulates both renal injury and T cell responses in MRLlpr mouse. C5aR-deficient MRLlpr mice had prolonged viability, with a mean survival time of 33.0 wk compared with 22.6 wk in control mice. Renal injury was also attenuated in the C5aR–/–MRLlpr mice. At 20 wk of age C5aR–/–MRLlpr mice had a complete absence of glomerular crescents and marked reductions in glomerular hypercellularity. There was no difference in the degree of glomerular C3 deposition; however, IgG deposits were reduced in the C5aR–/–MRLlpr mice. The reduction in glomerular injury was also associated with a four-fold decrease in renal CD4+ T cell infiltrates. Whereas there were modest differences in total IgG anti-dsDNA antibody titers, C5aR-deficient mice had 3.5-fold higher levels of IgG1 and 15-fold lower levels of IgG2a anti-dsDNA antibody titers compared to controls. The differences in anti-dsDNA IgG subclasses were associated with reduced CD4+ Th-1 responses in the C5aR–/–MRLlpr mice, including diminished production of IL-12p70, IFN-{gamma}, and increased expression of the Th-2 transcription factor GATA-3. These findings indicate that the C5aR plays a major role in modulating complement-dependent renal injury and T helper cell Th-1 responses in the MRLlpr mouse.


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