Kaufmann S H, Flesch I E, Munk M E, Wand-Württenberger A, Schoel B, Koga T
Department of Medical Microbiology and Immunology, University of Ulm, Federal Republic of Germany.
Rheumatol Int. 1989;9(3-5):181-6. doi: 10.1007/BF00271877.
Mycobacteria are intracellular pathogens capable of replicating in resting macrophages. Specific helper T lymphocytes which activate antimycobacterial capacities in infected macrophages represent an important constituent of acquired resistance. In addition, cytolytic T lymphocytes may contribute to resistance. On the other hand, lysis of infected host cells may also comprise autoaggressive consequences. Recent evidence suggest that T cells with specificity for mycobacterial heat shock proteins are involved in the antimycobacterial immune response. Heat shock proteins are evolutionarily highly conserved and cross-reactivity between microbial and mammalian molecules may occur on the B-cell and T-cell level. Thus, T cells directed against shared epitopes of mycobacterial and autologous origin could initiate autoimmune reactions.
分枝杆菌是能够在静止巨噬细胞中复制的细胞内病原体。在受感染巨噬细胞中激活抗分枝杆菌能力的特异性辅助性T淋巴细胞是获得性抗性的重要组成部分。此外，细胞毒性T淋巴细胞可能有助于产生抗性。另一方面，受感染宿主细胞的裂解也可能产生自身攻击的后果。最近的证据表明，对分枝杆菌热休克蛋白具有特异性的T细胞参与了抗分枝杆菌免疫反应。热休克蛋白在进化上高度保守，微生物和哺乳动物分子之间的交叉反应可能发生在B细胞和T细胞水平。因此，针对分枝杆菌和自身来源共同表位的T细胞可能引发自身免疫反应。
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