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The 30-kDa and 38-kDa antigens from Mycobacterium tuberculosis induce partial maturation of human dendritic cells shifting CD4+ T cell responses towards IL-4 production

机译:结核分枝杆菌的30-kDa和38-kDa抗原诱导人树突状细胞部分成熟,从而使CD4 + T细胞对IL-4产生的反应转移

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摘要

Background Mycobacterium tuberculosis (Mtb) infections are still a major cause of death among all infectious diseases. Although 99% of individuals infected with Mtb develop a CD4+ Th1 and CD8+ T cell mediated immunity as measured by tuberculin skin test, this results only in partial protection and Mtb vaccines are not effective. Deviation of immune responses by pathogens towards a Th2 profile is a common mechanism of immune evasion, typically leading to the persistence of the microbes.
机译:背景技术结核分枝杆菌(Mtb)感染仍然是所有传染病中死亡的主要原因。尽管通过结核菌素皮肤试验测定,有99%的Mtb感染者会形成CD4 + Th1和CD8 + T细胞介导的免疫力,但这只能部分保护,而Mtb疫苗则无效。病原体对Th2谱的免疫反应偏离是逃避免疫的常见机制,通常会导致微生物的持久性。

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