Abstract

The CD5(+) B cell population is prominent in early life and produce low avidity and, thereby, polyreactive antibodies. CD5(+) B cells are receptive to cytokines and interleukin-10 seems to be influential in the regulation of some of these CD5(+) B cells. The question of whether CD5 is a marker of activation or a molecule specific for a B cell lineage remains unresolved because evidence in support or against a separate lineage are still a matter for debate. However, we suggest the possibility of different kind of CD5(+) B cells. Indeed, activated CD5(+) B cells do proliferate, following CD5 engagement, while resting CD5(+) B cells do not. Moreover, three ligands for CD5 have, thus far, been identified but their functional effects are yet unknown. CD5(+) B cells probably play a role in setting up the idiotype network, antigen presentation and tolerance induction. B cells of most of the chronic lymphoid leukemias express CD5 molecules and, surprisingly, these cells may be expanded in non-organ-specific autoimmune diseases, such as rheumatoid arthritis or primary Sjögren's syndrome. CD5(+) B cells seems to be involved in the autoantibody production (this does not necessarily imply that pathogenic autoantibodies are produced by CD5(+) B cells) in autoimmune disease and particularly susceptible to transformation in lymphoproliferative disorders. Thus, this B cell population appears to play a key role at the crossroad of the non-organ-specific autoimmune diseases and B lymphoproliferative disorders.

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