01705nas a2200181   4500000000100000008004100001653001200042653004200054653003100096653002200127653002100149100001100170245006200181856003100243300001100274490000600285520123200291       2016                            d10aleprosy10aRegulatory T cells (Tregs) in leprosy10aT helper (Th)17 in leprosy10aLeprosy reactions10aT cell functions1 aNath I00aImmunopathogenesis of Leprosy: A Model for T Cell Anergy   uhttp://tinyurl.com/kyko9ky  a95-1010 v43 a<p>Leprosy is a model disease for understanding human immune responses underlying diseases caused by intracellular pathogens, as well as providing valuable insights into autoimmune disorders and cancer. This review addresses the unresponsiveness/anergy of host T cells to the causative pathogen Mycobacterium leprae and describes both the adaptive and innate immune responses observed during the clinical course of the disease. Leprosy presents as a clinicopathological spectrum, with divergence in antigen-specific T cell responses and antibodies in patients at the two ends of the spectrum. Tuberculoid leprosy at one end presents with localised hypopigmented paucibacillary skin patches, and shows effective antigenspecific T cell responses and low antibodies. In contrast, lepromatous leprosy at the other end presents with generalised lesions with bacillary proliferation, abundant antibodies, and T cell unresponsiveness/anergy to M. leprae. Recent advances that may explain clinical divergence and T cell unresponsiveness/anergy associated with lepromatous leprosy include: cytokine dysregulation, T helper (Th)1, Th2 paradigm, Th17 cells, FOXP3+ regulatory T cells, and pathogen-induced accessory cell subversion.</p>