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注射重组病毒蛋白后小鼠体内CD8 + T淋巴细胞介导的抗病毒免疫。

CD8+ T lymphocyte-mediated antiviral immunity in mice as a result of injection of recombinant viral proteins.

作者信息

Weidt G, Utermöhlen O, Zerrahn J, Reimann J, Deppert W, Lehmann-Grube F

机构信息

Heinrich-Pette Institute for Experimental Virology and Immunology, Hamburg University, Germany.

出版信息

J Immunol. 1994 Sep 15;153(6):2554-61.

PMID:8077665
Abstract

A major portion of the nucleoprotein (amino acids 67 through 300) and the glycoprotein-2 of lymphocytic choriomeningitis (LCM) virus were synthesized by using recombinant technology and were injected together with SDS twice in portions of 5 micrograms into BALB/c mice. As evidenced by diminished replication of LCM challenge virus, both proteins induced antiviral immunity, which was comparable in extent with the immunity caused by infection with LCM vaccinia recombinant viruses. Primed LCM-viral CTLs could not be demonstrated in these mice by culturing splenocytes in the presence of LCM virus, and Abs appeared slowly and in low quantities; but, after injection of large infectious doses, CTLs appeared faster and in higher numbers than in mice not previously treated with viral proteins. Depletion of CD8+ cells, but not of CD4+ cells, by treatment of mice with mAb abolished the antiviral immunity, demonstrating that protection was mediated by CD8+ T lymphocytes. Absence of CD4+ T lymphocytes before and during the period of immunization did not measurably affect the animals' antiviral immune status, indicating that activation of the CD8+ T lymphocytes was not dependent on help by CD4+ cells.

摘要

利用重组技术合成了淋巴细胞性脉络丛脑膜炎(LCM)病毒的大部分核蛋白(氨基酸67至300)和糖蛋白-2,并将其与SDS一起,分两次,每次5微克注射到BALB/c小鼠体内。如LCM攻击病毒复制减少所证明的,这两种蛋白均诱导了抗病毒免疫,其程度与LCM痘苗重组病毒感染所引起的免疫相当。在这些小鼠中,通过在LCM病毒存在的情况下培养脾细胞,无法证明有预先致敏的LCM病毒特异性CTL,而且抗体出现缓慢且数量少;但是,注射大剂量感染性病毒后,CTL出现得更快,数量也比未预先用病毒蛋白处理的小鼠更多。用单克隆抗体处理小鼠,使CD8⁺细胞而非CD4⁺细胞耗竭,消除了抗病毒免疫,表明这种保护是由CD8⁺T淋巴细胞介导的。免疫前和免疫期间缺乏CD4⁺T淋巴细胞对动物的抗病毒免疫状态没有明显影响,表明CD8⁺T淋巴细胞的激活不依赖于CD4⁺细胞的辅助。

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