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T Cells in Systemic Lupus erythematosus

Systemic lupus erythematosus (SLE) is characterized by generalized autoimmunity towards many organs and involves B cell hyperactivity, autoantibody production and deposits of immune complexes in vital organs. Tolerance to antigens ceases at the onset of the disease, but the mechanisms leading to it are still unknown and may be diverse. Nonetheless, an increasing body of evidence points to the critical role of distinctive CD4+ T cells in driving the B cell hyperactivity responsible for autoantibody hyperproduction. Thus two main questions should be addressed to further study human SLE: the origin of the immune dysregulation which leads to the end of tolerance and the autoantigens recognized by autoreactive T cells at the onset of the disease. For obvious reasons most of the concepts concerning immune dysregulation in SLE have been derived from the study of murine models of SLE, such as the MRL lpr/lpr mice. MRL mice homozygous for the lpr mutation (lpr is for lymphoproliferation) spontaneously develop a precocious SLE-like autoimmune disease with vasculitis and immune-complex glomerulonephritis and nonmalignant CD4‐8‐ T cell proliferation. Since the autoimmune