Complement and arthritis: another step in understanding
- PMID: 18304382
- PMCID: PMC2374468
- DOI: 10.1186/ar2359
Complement and arthritis: another step in understanding
Abstract
In a recent research article in Arthritis Research and Therapy ('Analysis of C204 and the C4 binding protein in the MRL/lpr mouse'), Wenderfer and colleagues report that deficiency in C4 binding protein, a down-regulator of the classic pathway of complement, does not affect the development of autoimmune disease. These data support the earlier finding that the alternative pathway, and not the classic pathway, drives disease progression. However, in a milder variant of the MRL/lpr model, the lpr/lpr mouse, classic pathway deficiency does contribute toward renal pathology and more severe disease. In this editorial we discuss the factors that may cause such a discrepancy.
Comment on
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Analysis of C4 and the C4 binding protein in the MRL/lpr mouse.Arthritis Res Ther. 2007;9(5):R114. doi: 10.1186/ar2320. Arthritis Res Ther. 2007. PMID: 17971229 Free PMC article.
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References
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- Watson ML, Rao JK, Gilkeson GS, Ruiz P, Eicher EM, Pisetsky DS, Matsuzawa A, Rochelle JM, Seldin MF. Genetic analysis of MRL-lpr mice: relationship of the Fas apoptosis gene to disease manifestations and renal disease-modifying loci. J Exp Med. 1992;176:1645–1656. doi: 10.1084/jem.176.6.1645. - DOI - PMC - PubMed
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