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感染MHV3的C57BL/6小鼠外周淋巴细胞中一些Vβ+ T细胞的克隆清除。

Clonal deletion of some V beta+ T cells in peripheral lymphocytes from C57BL/6 mice infected with MHV3.

作者信息

Gagne S, Thibodeau L, Lamontagne L

机构信息

Centre de Recherche en Virologie, Institut Armand-Frappier, Laval, Québec, Canada.

出版信息

Adv Exp Med Biol. 1998;440:485-9. doi: 10.1007/978-1-4615-5331-1_62.

Abstract

Mouse hepatitis virus type 3 infection is generally accompanied by a severe immune dysfunction involving thymic or splenic T cell subpopulations. We postulate that the peripheral lymphoid cell depletions were caused by a selective deletion of some V beta subsets of mature T cells, as observed with superantigens. We have examined the expression of V beta 6, V beta 8 and V beta 14 in T cell subpopulations from the spleen and lymph nodes of pathogenic L2-MHV3-infected C57BL/6 mice. Cytofluorometric study showed decreases in splenic V beta 8+, V beta 6+, and V beta 14+ T cell subpopulations at 72 hrs post-infection. Single positive CD4+ T cells were diminushed but not the CD8+ cells. In contrast, the various V beta splenic cell populations were not modified in mice infected with a non- pathogenic YAC-MHV3 variant. However, the V beta 8/CD4 ratio increased in splenic cells but decreased in lymphocytes from lymph nodes. The V beta 14/CD4 ratio decreased only in splenic cells while V beta 6/CD4 ratios were not modified. These results suggest that alterations in V beta cell populations may play a role in the L2-MHV3-induced immunodeficiency.

摘要

3型小鼠肝炎病毒感染通常伴随着严重的免疫功能障碍,涉及胸腺或脾脏的T细胞亚群。我们推测外周淋巴样细胞耗竭是由成熟T细胞某些Vβ亚群的选择性缺失引起的,这与超抗原的情况类似。我们检测了致病性L2-MHV3感染的C57BL/6小鼠脾脏和淋巴结T细胞亚群中Vβ6、Vβ8和Vβ14的表达。细胞荧光分析显示,感染后72小时,脾脏中Vβ8+、Vβ6+和Vβ14+T细胞亚群减少。单阳性CD4+T细胞减少,但CD8+细胞未减少。相比之下,感染非致病性YAC-MHV3变体的小鼠脾脏中各种Vβ细胞群体未发生改变。然而,脾脏细胞中Vβ8/CD4比值升高,而淋巴结淋巴细胞中该比值降低。Vβ14/CD4比值仅在脾脏细胞中降低,而Vβ6/CD4比值未改变。这些结果表明,Vβ细胞群体的改变可能在L2-MHV3诱导的免疫缺陷中起作用。

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