Advances of the Th1 Cell Immune Response of Brucella
Brucellosis is a zoonotic infectious disease caused by Brucella infection.Due to the ability of Brucella to survive in macropha-ges and other host cells,Th1 immune response is more important than Innate immune response in the host's adaptive immunity caused by Brucella infection.After phagocytosis of antigens,mononuclear macrophages present and produce a series of cytokines to CD4+T lymphocytes,activating CD4+T cells and triggering cellular immunity.Activated CD4+T cells further differentiate into Th1 cells,which produce interferon gamma(IFN-γ)through the JAK2/STAT1 signaling pathway to promote the secretion of CXCL9,CXCL10,and CXCL11 by white blood cells,macrophages,and fibroblasts.After binding to their receptors CXCR3 on Th1 cells,they attract more Th1 cells to secrete IFN-γ,activating the bactericidal activity of macrophages and CTL mediated cytotoxicity to limit Brucella infec-tion,thereby forming an amplification loop of Th1 immune response.This article will provide a brief summary of the mechanism of ac-tion of Brucella in innate and adaptive immune responses,as well as the immune regulation mechanism of IFN-γ in adaptive immunity,the regulation of IFN-γ and JAK-STAT signaling cascade and the role of receptors,and the role and related mechanisms of IFN-γ in-duced CXCL9,CXCL10,and CXCL11/CXCR3 axes.
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