Abnormalities in autologous mixed lymphocyte reaction‐activated immunologic processes in systemic lupus erythematosus and their possible correction by interleukin 2

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Abstract
The autologous mixed lymphocyte reaction (AMLR) represents the activation, proliferation and differentiation of T cells in response to signals from autologous non-T cells. Upon stimulation by autologous non-T cells, OKT4+ cells produce interleukin 2 (IL2); cells contained within both OKT4+ and OKT8+ cell populations can also be activated by autologous non-T cells to become sensitive to IL2. Once these activated OKT4+ and OKT8+ cells are exposed to IL2 produced by OKT4+ cells, they will proliferate and go on to differentiate into effector cells. Patients with systemic lupus erythematosus (SLE) have a defect in the AMLR. The ability of OKT4+ cells to produce IL 2 in the AMLR is impaired. Upon triggering with autologous non-T cells, their OKT8+ cells become sensitive to proliferative signals of IL2; however, their OKT4+ cells fail to express IL2 receptors. These defects are a consistent feature in patients with SLE. AMLR-induced immunologic processes which require cell interactions between OKT4+ cell subpopulations are not correct- able even by the addition of normal IL2. However, the immunologic processes medi ated through OKT4+-OKT8+ cell interactions can be corrected with normal 1L2. The latter finding suggests that the partial correction of the AMLR-induced immunologic processes with IL 2 might lead to suppressed B cell hyperactivity of patients with SLE.