Abstract
An autologous mixed lymphocyte reaction may be pathways for the activation of OKT 8+ cells via the interaction with OKT 4+ cells and for the cellular interactions between OKT 4+ subpopulations. Upon stimulation by autologous non-T cells, OKT 4+ helper T cells are activated to produce interleukin 2 (IL 2). Autologous non-T cells also render helper-effector function to these cells. Cells contained within OKT 4+ and OKT 8+ suppressor precursors can be activated by autologous non-T cells to express IL 2 receptors on their surface. IL 2 produced by OKT 4+ helper cells stimulates these cells bearing IL 2 receptors, facilitates their proliferation, and leads them to undergo differentiation into suppressor-effector cells. OKT 4+ helper cells, and OKT 4+ and OKT 8+ suppressor cells are in equilibrium in normal individuals and induce a normal B cell response.In patients with systemic lupus erythematosus (SLE), OKT 4+ helper T cells are defective with regard to their ability to produce IL 2; their helper function, however, is rather accelerated, so that upon activation in the AMLR, these cell populations can provide sufficient helper activity. Decreased production of IL 2 and the consequent loss of suppression cause the activation of B cells by uncontrolled OKT 4+ helper cells. SLE OKT 4+ cells have an additional defect. The OKT 4+ suppressor cells can not express IL 2 receptors during the AMLR activation. In contrast, SLE OKT 8+ suppressor cells are capable of expressing IL 2 receptors normally after stimulation with autologous non-T cells. Thus, the immunoregulatory circuits activated via cellular interactions between OKT 4+ cell subsets are completely defective in patients with SLE, indicating that this defect can not be correctable with addition of IL 2, whereas the defect in the circuits activated via cellular interactions between OKT 42 and OKT 8+ cells can be corrected with normal IL 2. The latter finding suggests that through the partial correction of immunoregulatory circuits with IL 2, B cell hyperactivity of patients with SLE could be suppressed.
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