The role of abnormal numbers and function of lymphocyte subsets in SLE remains, to date, unclear. Evidence exists for both functional T lymphocyte and B lymphocyte defects although the data for T lymphocyte defects appear more compelling. The role of autoantibodies on these cellular defects is also unclear. They may take on an important pathophysiologic role in depletion of certain lymphocyte subsets with subsequent alteration of function or they may, in fact, be interesting epiphenomena since an inverse relationship of depressed T lymphocyte numbers and function to increased levels of LCTA are frequent. Many other factors clearly influence lymphocyte function and disease expression including genetics and endocrine factors. As methodologies improve, a clearer understanding of the pathogenesis of SLE will emerge.