Mason U G, Kirkpatrick C H
J Clin Immunol. 1984 Mar;4(2):112-7. doi: 10.1007/BF00915044.
We have previously reported that impaired in vitro cellular immunity is a common finding in patients with nontuberculous mycobacterioses and that the subnormal responses may be improved by indomethacin. Subsequently, we have studied the in vivo effects of indomethacin on cell-mediated immune functions of four patients with Mycobacterium avium-intracellulare infections. Prior to treatment none of the patients had delayed cutaneous reactions to purified protein derivative (PPD) of the tubercle bacillus, and their lymphocytes had subnormal in vitro proliferation responses to tuberculins from M. tuberculosis and M. avium-intracellulare and to phytohemagglutinin. The administration of indomethacin reconstituted both the in vitro lymphocyte responses and delayed cutaneous hypersensitivity. We propose that the impairment of T-cell dependent immune functions is mediated by a suppressive factor (or factors) that is a metabolic product(s) of the cyclooxygenase pathway of arachidonic acid metabolism. Preferential inhibition of this pathway with indomethacin allows the expression of cell-mediated responses.
我们之前曾报道，体外细胞免疫受损在非结核分枝杆菌病患者中是常见现象，且消炎痛可能改善这种反应低下的情况。随后，我们研究了消炎痛对4例鸟分枝杆菌-胞内分枝杆菌感染患者细胞介导免疫功能的体内作用。治疗前，所有患者对结核杆菌纯蛋白衍生物（PPD）均无延迟性皮肤反应，其淋巴细胞对结核分枝杆菌、鸟分枝杆菌-胞内分枝杆菌的结核菌素以及植物血凝素的体外增殖反应均低于正常水平。消炎痛的给药恢复了体外淋巴细胞反应和延迟性皮肤超敏反应。我们提出，T细胞依赖性免疫功能的损害是由一种抑制因子（或多种因子）介导的，该抑制因子是花生四烯酸代谢环氧化酶途径的代谢产物。用消炎痛优先抑制该途径可使细胞介导反应得以表达。
