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• W2032256593 abstract "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." @default.
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• W2032256593 date "1985-01-01" @default.
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• W2032256593 title "Abnormalities in autologous mixed lymphocyte reaction-activated immunologic processes in systemic lupus erythematosus and their possible correction by interleukin 2" @default.
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• W2032256593 doi "https://doi.org/10.1002/eji.1830150310" @default.
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