New findings in the pathogenesis of leprosy and implications for the management of leprosy

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Purpose of review

This review focuses on recent work in leprosy pathogenesis. New research of both innate and adaptive immune responses to Mycobacterium leprae is described. The proposition that Mycobacterium lepromatosis is a new species causing leprosy is discussed.

Recent findings

Modulation of the lipid metabolism and reprogramming of adult Schwann cells have both been suggested as mechanisms used by M. leprae to disseminate the disease. New markers associated with localized, disseminated disease or the occurrences of leprosy reactions include the human interferons, CD163, microRNA-21, NOD2, galectin-3 and toll-like receptor 4. The role of keratinocytes instead of macrophages is underlined in the pathogenesis of leprosy. Adaptive immunity reports focus on the role of T regulatory cells and cytokines secreted by T helper cells in leprosy. Finally, a newly identified species named M. lepromatosis has been detected in patients with leprosy and severe erythema nodosum leprosum.


Novel biological pathways have been identified to be associated with the clinical phenotype of leprosy or the occurrence of leprosy reactions. Future work should include larger numbers of clinical samples from across the leprosy spectrum in order to give new insights in the pathogenesis and management of the disease.

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