Autoantibodies against complement C1q specifically target C1q bound on early apoptotic cells

December 2009
International Journal of Advances in Rheumatology;2009, Vol. 7 Issue 4, p123
Academic Journal
A major breakthrough in the understanding of the pathogenesis of systemic lupus erythematosus (SLE) is the "waste-disposal" hypothesis, which suggests that, in SLE, apoptotic cells can become antigenic and subsequently drive autoantibody production. Anti-complement component C1q (anti-C1q) antibodies have been intensively studied in SLE because their levels correlate with disease activity (especially nephritis), C1q-deficient individuals develop a lupus-like syndrome, and many SLE patients develop hypocomplementemia with depletion of C1q. These authors demonstrated that anti-C1q antibodies specifically target C1q that is bound to apoptotic cells. This suggests an intriguing link between C1q and the "waste disposal" hypothesis.


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