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DNA疫苗接种后体内维持Th1免疫的要求:CD8 + T细胞的潜在免疫调节作用。

Requirements for the maintenance of Th1 immunity in vivo following DNA vaccination: a potential immunoregulatory role for CD8+ T cells.

作者信息

Gurunathan S, Stobie L, Prussin C, Sacks D L, Glaichenhaus N, Iwasaki A, Fowell D J, Locksley R M, Chang J T, Wu C Y, Seder R A

机构信息

Clinical Immunology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Niational Institutes of Health, Bethesda, MD 20892, USA.

出版信息

J Immunol. 2000 Jul 15;165(2):915-24. doi: 10.4049/jimmunol.165.2.915.

Abstract

Protective immunity against Leishmania major generated by DNA encoding the LACK (Leishmania homologue of receptor for activated C kinase) Ag has been shown to be more durable than vaccination with LACK protein plus IL-12. One mechanism to account for this may be the selective ability of DNA vaccination to induce CD8+ IFN-gamma-producing T cells. In this regard, we previously reported that depletion of CD8+ T cells in LACK DNA-vaccinated mice abrogated protection when infectious challenge was done 2 wk postvaccination. In this study, we extend these findings to study the mechanism by which CD8+ T cells induced by LACK DNA vaccination mediate both short- and long-term protective immunity against L. major. Mice vaccinated with LACK DNA and depleted of CD8+ T cells at the time of vaccination or infection were unable to control infection when challenge was done 2 or 12 wk postvaccination. Remarkably, it was noted that depletion of CD8+ T cells in LACK DNA-vaccinated mice was associated with a striking decrease in the frequency of LACK-specific CD4+ IFN-gamma-producing T cells both before and after infection. Moreover, data are presented to suggest a mechanism by which CD8+ T cells exert this regulatory role. Taken together, these data provide additional insight into how Th1 cells are generated and sustained in vivo and suggest a potentially novel immunoregulatory role for CD8+ T cells following DNA vaccination.

摘要

编码活化C激酶受体的利什曼原虫同源物(LACK)抗原的DNA所产生的针对硕大利什曼原虫的保护性免疫,已被证明比用LACK蛋白加白细胞介素-12进行疫苗接种更持久。对此的一种解释机制可能是DNA疫苗接种诱导产生CD8⁺ 分泌干扰素-γ的T细胞的选择性能力。在这方面,我们之前报道过,在接种LACK DNA疫苗的小鼠中,接种后2周进行感染攻击时,CD8⁺ T细胞的耗竭会消除保护作用。在本研究中,我们扩展了这些发现,以研究LACK DNA疫苗接种诱导的CD8⁺ T细胞介导针对硕大利什曼原虫的短期和长期保护性免疫的机制。接种LACK DNA疫苗且在接种或感染时耗竭CD8⁺ T细胞的小鼠,在接种后2周或12周进行攻击时无法控制感染。值得注意的是,在接种LACK DNA疫苗的小鼠中,CD8⁺ T细胞的耗竭与感染前后LACK特异性CD4⁺ 分泌干扰素-γ的T细胞频率的显著降低有关。此外,还提供了数据以表明CD8⁺ T细胞发挥这种调节作用的机制。综上所述,这些数据为Th1细胞在体内如何产生和维持提供了更多见解,并提示了DNA疫苗接种后CD8⁺ T细胞潜在的新型免疫调节作用。

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