Stoner G L, Touw J, Belehu A, Naafs B
Lancet. 1978 Sep 9;2(8089):543-7. doi: 10.1016/s0140-6736(78)92881-7.
Lymphoproliferative responses to Mycobacterium leprae and P.P.D. were measured in 23 lepromatous and borderline lepromatous leprosy patients and in 27 of their normal siblings. At the same time siblings HLA-D-identical with the patients were identified by the absence of a mixed-lymphocyte reaction. The 7 siblings who were HLA-identical to lepromatous patients responded as well to M. leprae as did the 20 HLA-non-identical normal siblings. In contrast, 22 of the 23 lepromatous patients failed to respond to M. leprae but responded normally to P.P.D. The specific unresponsiveness of lepromatous patients thus does not result from an HLA-linked genetic defect and the defective cell-mediated immune response to M. leprae seems to be acquired, not inherited. Lepromatous patients may be high responders to antigens shared by M. leprae and other microorganisms in whom a strong antibody response has blocked the induction of an M. leprae-specific-cell-mediated immune response.
在23例瘤型和界线类偏瘤型麻风患者及其27名正常同胞中,检测了对麻风杆菌和结核菌素纯蛋白衍生物(PPD)的淋巴细胞增殖反应。同时,通过无混合淋巴细胞反应来鉴定与患者HLA - D相同的同胞。与瘤型患者HLA相同的7名同胞对麻风杆菌的反应与20名HLA不同的正常同胞一样。相比之下,23例瘤型患者中有22例对麻风杆菌无反应,但对PPD反应正常。因此,瘤型患者的特异性无反应并非由HLA连锁的基因缺陷导致,对麻风杆菌的细胞介导免疫反应缺陷似乎是后天获得的,而非遗传的。瘤型患者可能对麻风杆菌与其他微生物共有的抗原反应强烈,其中强烈的抗体反应阻断了麻风杆菌特异性细胞介导免疫反应的诱导。