Journal
IMMUNITY
Volume 16, Issue 2, Pages 157-168Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(02)00275-3
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Funding
- NCI NIH HHS [P50 CA86355] Funding Source: Medline
- NIAMS NIH HHS [1R01 AR/AI46580-01] Funding Source: Medline
- NIDDK NIH HHS [5 P30 DK36836-15] Funding Source: Medline
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Disease in these animals is focused specifically on the joints but stems from autoreactivity to a ubiquitously expressed antigen, glucose-6-phosphate isomerase (GPI). T and B cells are both required for disease initiation, but anti-GPI immunoglobulins; (Igs), alone, can induce arthritis in lymphocyte-deficient recipients. Here, we show that the arthritogenic Igs act through both Fc receptors (in particular, FcgammaRIII) and the complement network (C5a). Surprisingly, the alternative pathway of complement activation is critical, while classical pathway components are entirely dispensable. We suggest that autoimmune disease, even one that is organ specific, can occur when mobilization of an adaptive immune response results in runaway activation of the innate response.
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