02595nas a2200241   4500000000100000008004100001260001200042653003900054653002000093653002700113653002400140653001100164653001100175653002500186100001600211700001100227245013100238856007700369300001400446490000700460520187200467022001402339       2022                            d  c01/202210aCD4+CD25+FoxP3+ T regulatory cells10aTh1 cell anergy10aCell mediated immunity10alepromatous leprosy10aleptin10amTORC110atuberculosis leprosy1 aDegechisa S1 aDabi Y00aLeptin Deficiency May Influence the Divergence of Cell-Mediated Immunity Between Lepromatous and Tuberculoid Leprosy Patients.  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9758981/pdf/jir-15-6719.pdf  a6719-67280 v153 a<p>Leprosy is a disease caused by an intracellular bacillus bacterium called which lives and multiplies in the hosts' macrophages and Schwann cells. Depending on the degree of the host's cell-mediated immunity (CMI) response to the bacilli, the disease manifests itself in five clinical spectra ranging from polar tuberculoid (TT) to polar lepromatous leprosy (LL). A very high level of T helper 1 (Th1) driven bacilli-specific CMI is seen in the TT form, whereas this response is essentially nonexistent in the LL form. As a result, there is very low or absent bacillary load and localized nodular lesions in TT patients. On the contrary, LL patients presented with high bacillary load and generalized lesions due to low CMI response. The mechanism underlying this divergence of CMI response is not clearly elucidated yet. However, mounting evidence links it to an elevated number of Th1 and Th17 suppressing CD4 CD25 FOXP3 T regulatory cells (Treg cells) which are abundantly found in LL than in TT patients. The predominance of these cells in LL patients is partly attributed to a deficiency of leptin, the cytokine-like peptide hormone, in these patients. Becausea normal level of leptin promotes the proliferation and preferential differentiation of effector T cells (Th1 and Th17) while inhibiting the growth and functional responsiveness of the Treg cells. In contrast, leptin deficiency or neutralization was reported to exert the opposite effect on Treg cells and effector T cells. Other smaller subsets of lymphocytes such as gamma delta (γδ) T cells and B regulatory cells are also modulated by leptin level in the pathogenesis of leprosy. Leptin may therefore regulate the divergence of CMI between TT and LL patients by regulating the homeostasis of effector T cells and Treg cells, and this review will examine the underlying mechanism for this.</p>
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