43 RFM also enhances the production of NO, which might be respons

43 RFM also enhances the production of NO, which might be responsible for parasite killing.44 This was a comprehensive study carried out to investigate the abundance of localized and circulating cytokines in patients with CL caused by L. tropica. Furthermore, the study carried out a comparative assessment of different treatment regimens on the

host immune response, which will help to explore the action of chemotherapy. The higher production of IL-8 in CL patients, leading to excessive inflammatory cell activation, predominantly PMNs that provide shelter to parasites, may allow the parasite to survive and multiply, leading to the development of disease. The observation of high levels of NO and MCP-1 following treatment suggests that MCP-1 orchestrates the induction of leishmanicidal activities in human macrophages Cabozantinib via the generation

of NO. Financial assistance by the Indian Council of Medical Research is gratefully acknowledged. None of the authors of this paper have conflict of interest to disclose. “
“Natural killer (NK) cells are important components of the innate immune system that mediate effector and regulatory functions. As effector cells, NK cells help control virus-infected cells through cell-mediated antibody-dependent mechanisms such as antibody-dependent cellular cytotoxicity (ADCC). Although macaques are an important and reliable

animal model for the study of retrovirus-induced human diseases, and despite the crucial role played by NK cells in innate MK-2206 cell line and adaptive immune responses against simian immunodeficiency virus (SIV), only a few studies have attempted to characterize different macaque NK cell subpopulations. In the present study, we identified a subpopulation of circulatory CD8α− macaque NK cells that express NK lineage markers and exhibit cytotoxic potential. CD8α− NK cells were phenotypically characterized as CD3− CD14− CD20− CD8α− cells ID-8 that express NK cell markers including CD16, CD56, granzyme B, perforin, NKG2D and KIR2D. Based on their CD56/CD16 expression patterns, cells within the CD8α− gate can be divided into four subpopulations: CD56dim CD16bright, CD56dim CD16−, CD56bright CD16−, and CD56− CD16− cells. In contrast, CD8α+ NK cells are 95% CD56dim CD16bright, which correlates with their high cytotoxic potential. Upon interleukin-15 activation, CD8α− cells up-regulated CD69 expression and produced low levels of interferon-γ and tumour necrosis factor-α. Sorted CD8α− NK cells were capable of killing MHC-I-devoid target cells and mediated ADCC responses against SIV gp120-coated target cells in the presence of macaque anti-gp120 antibodies.

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