The role of Schwann cells, T cells andMycobacterium lepraein the immunopathogenesis of nerve damage in leprosy

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-l T cells has been suggested.Mycobacterium Zeprae 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. Zeprae, 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. Zeprae to antigen-specific, inflammatory, type-l 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 + Thl cells in the lesions of leprosy.Antagonism of the molecular inter actions among M. Zeprae, Schwann cells and inflammatory T cells may therefore provide a rational strategy for prevention of damage of Schwann cell and nerves in leprosy. Leprosy reactions and nerve damageLeprosy is the leading cause of all non-traumatic peripheral neuropathies worldwide.I Although the implementation of multidrug therapy (MDT) has caused a major decline of the prevalence of leprosy wOrldwide, 2 the new-case detection rate has remained stable at a level of approximately 600,000 annually.It is well established that host immunity to My cobacterium Zeprae dictates the clinical outcome of leprosy.It is believed that more than 99% of the population develop adequate protective immunity upon infection, and do not develop clinically detectable symptoms, 3 ,4 and only a minority of the infected individuals develop clinical leprosy.