Indomethacin enhances the proliferation of mitogen-stimulated T lymphocytes of homosexual males with persistent generalized lymphadenopathy.

The possibility that cyclooxygenase products of arachidonic acid might contribute to the defective T lymphocyte function of homosexual men with the reactive lymph node syndrome was examined in vitro. T lymphocyte proliferation, assessed by the uptake of [3H]thymidine after the addition of phytohemagglutin, was 72,870 +/- 66,816 counts per minute (mean +/- SD) for eight patients and 119,589 +/- 64,913 counts per minute for 30 controls (P less than 0.05, Student's t test). Treatment with the cyclooxygenase inhibitor indomethacin increased the phytohemagglutin-induced proliferation of the T lymphocytes from five of eight patients, but none of 12 healthy homosexual and heterosexual control subjects. The production of prostaglandin E2 by T lymphocytes from six patients was 16.1 +/- 10.5 pg/5 X 10(6) cells/hr, as contrasted with that of 4.9 +/- 1.3 and 4.3 +/- 2.1 pg/5 X 10(6) cells for four healthy homosexual and six healthy heterosexual control subjects, respectively (P less than 0.01, Student's t test). The production of prostaglandin E2 by the patients' monocytes was normal. Abnormalities of the cyclooxygenase pathway of T lymphocytes of patients with the reactive lymph node syndrome may reflect an immunoregulatory defect, which predisposes to infections and may evolve into the more severe abnormalities of the acquired immune deficiency syndrome.