Patients with SLE have excessive B cell proliferation. They have increased proliferation of bone marrow stem cells and circulating B cell precursors. Disease activity is characterized by a switch from just proliferation to differentiation and immunoglobulin synthesis. In some patients the T cell regulation of B cell functions is abnormal. In an attempt to better understand cell-cell inter-actions, normals were studied for the capacity of T cells to respond to autologous non-T cells. IL 2 production by T4 plus cells was necessary for the proliferation of T8 plus (suppressor) cells. This function is subnormal in patients with SLE. Monoclonal antibodies were used to study subpopulations of SLE patients. One subset, with a reduced ratio of helper/suppressor cells, was characterized clinically by renal disease, thrombocytopenia, leukopenia and early age of onset of disease. Another subset had a high ratio and a clinical picture which included muscle and lung disease, Sicca syndrome, lympadenopathy and CNS disease. Thus, SLE may not be a single disease, but a group of syndromes with different genetic and cellular bases. SLE patients have a variety of T cell defects. These are largely explained by anti-T cell antibodies produced by the B cells of these patients. The more rapidly progressive autoimmune lymphorproliferative disorder, angioimmunoblastic lymphadenopathy is characterized by markedly effective helper T cells which drive B cells to proliferate and differentiate. The B cells themselves are normal in this varient. Proto-oncogene expression is abnormal in patients with SLE. There is a significant increase in expression characteristic of activated B cells.
