Abstract
The neurotropism of Mycobacterium leprae is a unique characteristic that distinguishes it from other mycobacteria. However, the mechanism of peripheral nerve injury in leprosy is still unclear. In this study, immunohistochemistry and qPCR found that skin lesions from people with leprosy expressed IL-22 at a significantly higher rate than other mycobacterium-infected skin lesions, and that IL-22 was concentrated around the cutaneous nerves. Further investigation found that IL-22 is involved in leprosy by regulating neuroinflammation and promoting apoptosis via the JAK-STAT pathway.
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