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九英里一期原发性感染产生的针对 C. 再感染的保护免疫依赖于 B 细胞和 T 细胞,但 T 细胞发挥关键作用。

Nine Mile phase I primary infection derived protective immunity against C. reinfection in mice depends on both B and T cells, but T cells play a critical role.

机构信息

Department of Molecular Microbiology and Immunology, The University of Texas at San Antonio, San Antonio, TX, United States.

Department of Microbiology, Immunology and Molecular Genetics, The University of Texas Health Science Center San Antonio, San Antonio, TX, United States.

出版信息

Front Immunol. 2024 Oct 14;15:1427822. doi: 10.3389/fimmu.2024.1427822. eCollection 2024.

Abstract

is an obligate intracellular Gram-negative bacterium that causes acute and chronic Q fever in humans. Acute Q fever is usually a flu-like, self-limiting or treatable illness, but some infections can turn into a severe and sometimes fatal chronic disease. There is currently no FDA-approved vaccine available for the prevention of human Q fever in the US, development of a safe and effective vaccine for the prevention of human Q fever remains an important goal for public health. However, there is a fundamental gap in knowledge regarding the mechanism of protective immunity against infection. To understand the mechanism of infection induced protective immunity, we examined if Nine Mile phase I (NMI) infection induces protection against reinfection in mice. Our results indicate that NMI-infected mice conferred significant protection against reinfection. We also found that NMI infection derived protection did not depend on the routes of infection and antibodies are required for NMI infection derived protection. In addition, NMI infection elicited a comparable level of protection in Wild type, CD4 T cell deficient, and CD8 T cell deficient mice, partial protection in B cell deficient mice but no protection in T cell deficient mice. These results suggest that both B cells and T cells are required for NMI-infection derived protection, but T cells may play a critical role. Therefore, the new generation vaccine for the prevention of human Q fever should be focused on boosting both humoral and T cell immune responses.

摘要

它是一种专性细胞内革兰氏阴性菌,可导致人类急性和慢性 Q 热。急性 Q 热通常是一种类似流感的、自限性或可治疗的疾病,但有些感染可能会发展成严重的、有时甚至致命的慢性疾病。目前,美国没有 FDA 批准的疫苗可预防人类 Q 热,开发安全有效的疫苗预防人类 Q 热仍然是公共卫生的一个重要目标。然而,人们对 感染诱导保护性免疫的机制知之甚少。为了了解 感染诱导保护性免疫的机制,我们研究了 9 英里一期(NMI)感染是否能在小鼠中诱导对 再感染的保护。我们的结果表明,NMI 感染的小鼠对 再感染有显著的保护作用。我们还发现,NMI 感染衍生的保护并不依赖于感染途径,并且抗体是 NMI 感染衍生保护所必需的。此外,NMI 感染在野生型、CD4 T 细胞缺陷型和 CD8 T 细胞缺陷型小鼠中引起了相当水平的保护,在 B 细胞缺陷型小鼠中引起了部分保护,但在 T 细胞缺陷型小鼠中没有保护。这些结果表明,B 细胞和 T 细胞都需要 NMI 感染衍生的保护,但 T 细胞可能起着关键作用。因此,预防人类 Q 热的新一代疫苗应侧重于增强体液和 T 细胞免疫反应。

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