Samuel N M, Mirsky R, Grange J M, Jessen K R
Department of Microbiology, Cardiothoracic Institute, London, UK.
Clin Exp Immunol. 1987 Jun;68(3):500-9.
Recent experiments on rats have raised the possibility that Schwann cells can present antigens to T lymphocytes. We have investigated whether this mechanism might be relevant in leprosy by determining under what conditions human Schwann cells express class I and class II antigens, and whether infection with Mycobacterium leprae affects this expression. The distribution of these antigens was examined on human Schwann cells in dissociated cell cultures derived from human fetal peripheral nerves. We find that both Schwann cells and fibroblastic cells in these cultures normally express class I antigens but not class II antigens. When Schwann cells are infected with live Mycobacterium leprae for 48 h, 73% of Schwann cells phagocytose the bacteria. Mycobacterium leprae prevents 3H-thymidine incorporation into cultured human Schwann cells, but does not affect class I expression in these cells. Treatment of normal and Mycobacterium leprae infected cultures with gamma-interferon for 72 h induces class II expression on most Schwann cells but not on the majority of fibroblastic cells. The fact that human Schwann cells infected with Mycobacterium leprae can be induced by gamma-interferon to express class II antigens suggests that they may be able to present Mycobacterium leprae antigens to T lymphocytes and thus initiate immune responses against the bacteria. We suggest that a failure of this response, such as that seen within nerve trunks in lepromatous leprosy, is caused by deficient class II expression on Schwann cells. This deficiency in class II expression, in turn, may be caused by the reduced gamma-interferon production characteristic of lepromatous leprosy.
最近对大鼠进行的实验增加了施万细胞能够将抗原呈递给T淋巴细胞的可能性。我们通过确定人类施万细胞在何种条件下表达I类和II类抗原,以及麻风分枝杆菌感染是否会影响这种表达,来研究这种机制在麻风病中是否相关。在源自人类胎儿外周神经的解离细胞培养物中的人类施万细胞上检查了这些抗原的分布。我们发现这些培养物中的施万细胞和成纤维细胞通常都表达I类抗原,但不表达II类抗原。当施万细胞被活的麻风分枝杆菌感染48小时时,73%的施万细胞吞噬细菌。麻风分枝杆菌阻止3H-胸腺嘧啶核苷掺入培养的人类施万细胞中,但不影响这些细胞中的I类表达。用γ-干扰素处理正常和麻风分枝杆菌感染的培养物72小时可诱导大多数施万细胞表达II类抗原,但大多数成纤维细胞则不表达。感染麻风分枝杆菌的人类施万细胞可被γ-干扰素诱导表达II类抗原这一事实表明,它们可能能够将麻风分枝杆菌抗原呈递给T淋巴细胞,从而启动针对该细菌的免疫反应。我们认为,这种反应的失败,如在瘤型麻风的神经干中所见,是由于施万细胞上II类表达不足所致。反过来,这种II类表达的不足可能是由瘤型麻风特有的γ-干扰素产生减少引起的。