Bhattacharjee Surajit, Gupta Gaurav, Bhattacharya Parna, Adhikari Anupam, Majumdar Suchandra Bhattacharya, Majumdar Subrata
Indian J Exp Biol. 2009 Jun;47(6):489-97.
Visceral leishmaniasis is characterized by severe immune suppression of the host. This suppression of the host immune system is primarily mediated by the immunosuppressive cytokine Interleukin-10 (IL-10), whose levels are significantly upregulated during leishmaniasis. This immune suppression is reflected at the level of T-cell dysfunction and abrogation of leishmaniacidal molecules along with a dampened Th1 cytokine response. In the present study, we showed in vivo neutralization of IL-10 by administration of anti IL-10 monoclonal antibodies (mAb) could confer protection against leishmanial pathogenesis. This protective response was primarily mediated by a strong induction of T cell proliferation along with a Th1 biased cytokine response which was further aided by the generation of, leishmanicidal molecules, nitric oxide.
内脏利什曼病的特征是宿主严重免疫抑制。宿主免疫系统的这种抑制主要由免疫抑制细胞因子白细胞介素-10(IL-10)介导,其水平在利什曼病期间显著上调。这种免疫抑制反映在T细胞功能障碍和利什曼杀菌分子的消除水平上,同时Th1细胞因子反应减弱。在本研究中,我们表明通过给予抗IL-10单克隆抗体(mAb)在体内中和IL-10可以提供针对利什曼病发病机制的保护。这种保护性反应主要由T细胞增殖的强烈诱导以及Th1偏向的细胞因子反应介导,而利什曼杀菌分子一氧化氮的产生进一步促进了这种反应。