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在没有其他T细胞的情况下,反复的寄生虫感染可诱导γδT细胞对B细胞的辅助作用。

Gamma delta T cell help of B cells is induced by repeated parasitic infection, in the absence of other T cells.

作者信息

Pao W, Wen L, Smith A L, Gulbranson-Judge A, Zheng B, Kelsoe G, MacLennan I C, Owen M J, Hayday A C

机构信息

Department of Biology, Yale University, New Haven, Connecticut 06520, USA.

出版信息

Curr Biol. 1996 Oct 1;6(10):1317-25. doi: 10.1016/s0960-9822(02)70718-5.

Abstract

BACKGROUND

gamma delta T cells, like alpha beta T cells, are components of all well-studied vertebrate immune systems. Yet, the contribution of gamma delta T cells to immune responses is poorly characterized. In particular, it has not been resolved whether gamma delta cells, independent of any other T cells, can help B cells produce immunoglobulin and form germinal centers, anatomical foci of specialized T cell-B cell collaboration.

RESULTS

TCR beta-/- mice, which lack all T cells except gamma delta T cells, routinely displayed higher levels of antibody than fully T cell-deficient mice. Repeated parasitic infection of TCR beta-/- mice, but not of T cell-deficient mice, increased antibody levels and induced germinal centers that contained B cells and monoclonal gamma delta cells in close juxtaposition. However, antibody specificities were more commonly against self than against the challenging pathogen. gamma delta T cell-B cell help was not induced by repeated inoculation of TCR beta-/- mice with mycobacterial antigens.

CONCLUSIONS

In the absence of any other T cells, gamma delta T cell-B cell collaboration can be significantly enhanced by repeated infection. However, the lack of obvious enrichment for antibodies against the challenging pathogen distinguishes gamma delta T cell help from alpha beta T cell help induced under analogous circumstances. The increased production of generalized antibodies may be particularly relevant to the development of autoimmunity, which commonly occurs in patients suffering from alpha beta T cell deficiencies, such as AIDS.

摘要

背景

γδT细胞与αβT细胞一样,是所有经过充分研究的脊椎动物免疫系统的组成部分。然而,γδT细胞对免疫反应的贡献却鲜为人知。特别是,γδ细胞能否独立于任何其他T细胞帮助B细胞产生免疫球蛋白并形成生发中心(专门的T细胞 - B细胞协作的解剖学部位),这一问题尚未得到解决。

结果

TCRβ-/-小鼠除γδT细胞外缺乏所有T细胞,其抗体水平通常高于完全缺乏T细胞的小鼠。TCRβ-/-小鼠反复受到寄生虫感染(而非T细胞缺陷小鼠)会增加抗体水平并诱导生发中心形成,生发中心中B细胞和单克隆γδ细胞紧密相邻。然而,抗体特异性更常见地是针对自身而非攻击的病原体。用分枝杆菌抗原反复接种TCRβ-/-小鼠并不会诱导γδT细胞 - B细胞的辅助作用。

结论

在没有任何其他T细胞的情况下,反复感染可显著增强γδT细胞 - B细胞的协作。然而,针对攻击病原体的抗体缺乏明显富集,这将γδT细胞的辅助作用与在类似情况下诱导的αβT细胞的辅助作用区分开来。广义抗体产量的增加可能与自身免疫的发展特别相关,自身免疫常见于患有αβT细胞缺陷的患者,如艾滋病患者。

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