| Popis: |
B-cell hyperactivity is the general and cardinal feature of murine and human systemic lupus erythematosus (SLE), the prototype organ-non-specific autoimmune disease. The defect(s) responsible could be intrinsic to B cells, secondary to T-cell or macrophage abnormalities resulting in excessive help or deficient suppression, or could stem f rom qualitative/quantitative abnormalities of autoantigens. Here Argyrios Theofilopoulos and his colleagues review the immunopathological and cellular abnormalities observed in murine lupus and the factors currently thought to play a role in normal B-cell proliferation, differentiation and Ig class switching. Next month, in a second article, they discuss abnormalities in B-cell response to and/or overproduction of T-cell-derived accessory signals which may explain the generalized B-cell hyperactivity associated with mouse and human lupus. |
