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肽诱导CD8 + T细胞缺陷小鼠对Friend逆转录病毒诱导疾病的免疫保护。

Peptide-induced immune protection of CD8+ T cell-deficient mice against Friend retrovirus-induced disease.

作者信息

Kawabata Hiroyuki, Niwa Atsuko, Tsuji-Kawahara Sachiyo, Uenishi Hirohide, Iwanami Norimasa, Matsukuma Hideaki, Abe Hiroyuki, Tabata Nobutada, Matsumura Haruo, Miyazawa Masaaki

机构信息

Department of Immunology, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osaka-Sayama, Osaka 589-8511, Japan.

出版信息

Int Immunol. 2006 Jan;18(1):183-98. doi: 10.1093/intimm/dxh361. Epub 2005 Dec 13.

Abstract

CD8+ CTLs and virus-neutralizing antibodies have been associated with spontaneous and vaccine-induced immune control of retroviral infections. We previously showed that a single immunization with an env gene-encoded CD4+ T cell epitope protected mice against fatal Friend retrovirus infection. Here, we analyzed immune cell components required for the peptide-induced anti-retroviral protection. Mice lacking CD8+ T cells were nevertheless protected against Friend virus infection, while mice lacking B cells were not. Virus-producing cells both in the spleen and bone marrow decreased rapidly in their number and became undetectable by 4 weeks after infection in the majority of the peptide-immunized animals even in the absence of CD8+ T cells. In the vaccinated animals the production and class switching of virus-neutralizing and anti-leukemia cell antibodies were facilitated; however, virus-induced erythroid cell expansion was suppressed before neutralizing antibodies became detectable in the serum. Further, the numbers of virus-producing cells in the spleen and bone marrow in the early stage of the infection were smaller in the peptide-immunized than in unimmunized control mice in the absence of B cells. Thus, peptide immunization facilitates both early cellular and late humoral immune responses that lead to the effective control of the retrovirus-induced disease, but CD8+ T cells are not crucial for the elimination of virus-infected cells in the peptide-primed animals.

摘要

CD8+细胞毒性T淋巴细胞(CTL)和病毒中和抗体与逆转录病毒感染的自发免疫控制及疫苗诱导的免疫控制有关。我们之前表明,用env基因编码的CD4+ T细胞表位进行单次免疫可保护小鼠免受致命的Friend逆转录病毒感染。在此,我们分析了肽诱导的抗逆转录病毒保护所需的免疫细胞成分。缺乏CD8+ T细胞的小鼠仍能免受Friend病毒感染,而缺乏B细胞的小鼠则不能。即使在没有CD8+ T细胞的情况下,在大多数肽免疫的动物中,脾脏和骨髓中的病毒产生细胞数量在感染后4周迅速减少并变得无法检测到。在接种疫苗的动物中,病毒中和抗体和抗白血病细胞抗体的产生及类别转换得到促进;然而,在血清中可检测到中和抗体之前,病毒诱导的红系细胞扩增受到抑制。此外,在没有B细胞的情况下,肽免疫小鼠在感染早期脾脏和骨髓中病毒产生细胞的数量比未免疫的对照小鼠少。因此,肽免疫促进了早期细胞免疫和晚期体液免疫反应,从而有效控制逆转录病毒诱导的疾病,但CD8+ T细胞对于肽引发的动物中病毒感染细胞的清除并非至关重要。

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