Wadee A A, Sher R, Rabson A R
J Immunol. 1980 Sep;125(3):1380-6.
Human peripheral blood mononuclear cell (MN) proliferation and lymphokine production induced by mitogen could be inhibited by heat killed whole mycobacteria. The inhibition was induced by a wide variety of mycobacteri but not by other Gram-positive or Gram-negative organisms or by latex particles. Proliferation and lymphokine production by adherent cell-depleted lymphocytes was not inhibited by these organisms. Adherent cells treated with mycobacteria had the ability to inhibit lymphocyte blastogenesis when co-cultured with the lymphocytes. the inhibitory effect of these adherent cells was due to the release of a heat stable, nondialyzable suppressor cells. These latter cells, which were T gamma cells, could inhibit the blastogenic ability of normal lymphocytes activated by mitogens. The results suggest that in situations of high mycobacterial load, adherent cells are activted to release a suppressor factor that will activate lymphocytes to become suppressor cells. This mechanism may explain the anergy associated with lepromatous leprosy or advanced tuberculosis.
热灭活的全部分枝杆菌可抑制有丝分裂原诱导的人外周血单核细胞(MN)增殖及淋巴因子产生。多种分枝杆菌均可诱导这种抑制作用,但其他革兰氏阳性菌、革兰氏阴性菌或乳胶颗粒则无此作用。去除贴壁细胞的淋巴细胞的增殖及淋巴因子产生不受这些微生物的抑制。用分枝杆菌处理的贴壁细胞与淋巴细胞共培养时,具有抑制淋巴细胞母细胞形成的能力。这些贴壁细胞的抑制作用归因于一种热稳定、不可透析的抑制细胞的释放。这些后者的细胞为Tγ细胞,可抑制有丝分裂原激活的正常淋巴细胞的母细胞形成能力。结果表明,在分枝杆菌负荷高的情况下,贴壁细胞被激活以释放一种抑制因子,该因子将激活淋巴细胞成为抑制细胞。这一机制可能解释与瘤型麻风或晚期结核病相关的无反应性。