Infectious Diseases and Immunology Division, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology (CSIR-IICB), Kolkata, India.
Front Immunol. 2019 Apr 12;10:616. doi: 10.3389/fimmu.2019.00616. eCollection 2019.
Immunosuppression is a characteristic feature of chronic leishmaniasis. The dynamicity and the functional cross talks of host immune responses during infection are still not clearly understood. Here we explored the functional aspects of accumulation of immune suppressive cellular and cytokine milieu during the progression of murine visceral leishmaniasis. In addition to IL-10 and TGF-β, investigation on the responses of different subunit chains of IL-12 family revealed a progressive elevation of EBI-3 and p35 chains of EBI-3 with infection in BALB/c mice. The expansion of CD25 and FoxP3 positive T cells is associated with loss of IFN-γ and TNF-α response in advanced disease. and neutralization of TGF-β and EBI-3 suggests a synergism in suppression of host anti-leishmanial immunity. The down-regulation of EBI-3 and TGF-β is crucial for re-activation of JAK-STAT pathway for induction as well as restoration of protective immunity against infection.
免疫抑制是慢性利什曼病的一个特征。宿主免疫反应在感染过程中的动态性和功能串扰仍不清楚。在这里，我们研究了在感染期间积累免疫抑制性细胞和细胞因子环境的功能方面，在 BALB/c 小鼠中，除了 IL-10 和 TGF-β之外，对 IL-12 家族不同亚基链反应的研究表明，EBI-3 的 EBI-3 和 p35 链随着感染的进展而逐渐升高。CD25 和 FoxP3 阳性 T 细胞的扩增与晚期疾病中 IFN-γ和 TNF-α反应的丧失有关。中和 TGF-β和 EBI-3 提示抑制宿主抗利什曼原虫免疫具有协同作用。下调 EBI-3 和 TGF-β对于 JAK-STAT 途径的重新激活至关重要，这是诱导和恢复对 感染的保护性免疫所必需的。
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