Abstract
Our current understanding of the anti-Sm response is that it is SLE specific, antigen driven, and T cell dependent. It does not require a particular VH-VL Ig gene combination, but probably can be coded for by a limited number of such genes. It also appears in very high titers and in the isotypes which are characteristic of autoantibodies in autoimmune mice. Thus, the formation of anti-Sm antibodies in such mice probably reflects the basic immunoregulatory abnormalities that are fundamental to the spontaneous SLE syndrome in these animals.
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