Spierings E, De Boer T, Zulianello L, Ottenhoff T H
Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands.
Lepr Rev. 2000 Dec;71 Suppl:S121-9.
Damage to peripheral nerves is the major complication of reversal (type I) reactions in leprosy. The underlying mechanism of nerve damage remains largely unresolved; however, an important role for type-1 T cells has been suggested. Mycobacterium leprae has a remarkable tropism for the Schwann cells that surround peripheral axons. Because reversal reactions in leprosy are often accompanied by severe and irreversible nerve destruction, and are associated with increased cellular immune reactivity against M. leprae, a likely immunopathogenic mechanism of damage to Schwann cells and peripheral nerves in leprosy is that infected Schwann cells process and present antigens of M. leprae to antigen-specific, inflammatory, type-1 T cells, and that these T cells subsequently damage and lyse infected Schwann cells. Previous animal studies with CD8+ T cells revealed evidence for the existence of such a mechanism. A similar role has been suggested for CD4+ T cells. These latter cells may be more important in causing nerve damage in vivo, given the predilection of M. leprae for Schwann cells, and the dominant role of CD4+, serine esterase+ Th1 cells in the lesions of leprosy. Antagonism of the molecular interactions among M. leprae, Schwann cells and inflammatory T cells may therefore provide a rational strategy for prevention of damage of Schwann cell and nerves in leprosy.
周围神经损伤是麻风病逆转（I型）反应的主要并发症。神经损伤的潜在机制在很大程度上仍未得到解决；然而，已有人提出1型T细胞发挥重要作用。麻风杆菌对围绕周围轴突的施万细胞具有显著的嗜性。由于麻风病的逆转反应常伴有严重且不可逆的神经破坏，并且与针对麻风杆菌的细胞免疫反应性增加相关，因此麻风病中施万细胞和周围神经损伤的一种可能的免疫致病机制是，被感染的施万细胞处理并将麻风杆菌抗原呈递给抗原特异性、炎性的1型T细胞，随后这些T细胞损伤并裂解被感染的施万细胞。先前对CD8 + T细胞进行的动物研究揭示了存在这种机制的证据。对于CD4 + T细胞也提出了类似作用。鉴于麻风杆菌对施万细胞的偏好以及CD4 +、丝氨酸酯酶 + Th1细胞在麻风病病变中的主导作用，后一类细胞在体内引起神经损伤方面可能更为重要。因此，拮抗麻风杆菌、施万细胞和炎性T细胞之间的分子相互作用可能为预防麻风病中施万细胞和神经损伤提供一种合理策略。
