B lymphocytes in nonorgan-specific autoimmune diseases: implications for therapy

Abstract

Beyond the paradigm that T lymphocytes exert strict control over them, B lymphocytes have recently been assigned numerous functions. 1 Therefore, they are not confined anymore to anti- body production. Rather, evidence accumulates that they govern immune responses to self and non-self-antigen through antibody-dependent as well as antibody-independent mechanisms. An inference from such a sudden awareness is that systemic lupus erythematosus (SLE), rheuma- toid arthritis (RA) and primary Sjogren's syndrome (SS), long viewed as T cell-driven conditions, are being re-examined from the outset. Thus, this review ventures into the area of the relationships between autoimmune processes and B lymphocytes. The evidence that B cells are the culprits in SLE, RA and primary SS may be listed under three head- ings, following recent major breakthroughs in their study. The first is the demonstration that the CD5 molecule acts as a regulator for their activities; the second, the dissection of B-lymphocyte subsets; and the third, the report of two supplemental tumour- necrosis factor (TNF) family members. One is referred to as BAFF, for B cell-activating factor of the TNF family, and the other as APRIL, for a proliferation-inducing ligand. No doubt, develop- ing insights into B lymphocyte commitment in non- organ-specific autoimmune diseases should bring about new therapeutic approaches. The CD5 control of B lymphocytes A T cell marker has been found on the B cells from patients with chronic lymphocytic leukaemia, and subsequently identified as CD5. The B-cell