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[非结核分枝杆菌感染过程中γδTCR + T细胞的行为及宿主淋巴细胞对65kD热休克蛋白的增殖反应]

[Behaviour of gamma delta TCR+ T cells during the course of nontuberculous mycobacterial infections and proliferative response of host lymphocytes to 65kD heat shock protein].

作者信息

Tomioka H, Saito H, Emori M, Setogawa T

机构信息

Department of Microbiology and Immunology, Shimane Medical University, Japan.

出版信息

Kekkaku. 1993 Feb;68(2):99-104.

PMID:8479112
Abstract

In order to know the possibility that gamma delta TCR+ T cells induced by Mycobacterium avium complex (MAC) infections participate in the expression of host resistance and in the occurrence of Behçet disease, we examined the behaviour of them in MAC-infected host mice. In both BALB/c (Bcgs; MAC-susceptible) and CBA/JN (Bcgr; MAC-resistant) strain mice, a transient but appreciable increase in the number of gamma delta TCR+ T cells in the host peritoneal lymphocytes was noted around week 1 to 2 after M. intracellulare infection via ip. route. The degree of induction of gamma delta TCR+ T cells was somewhat higher in CBA/JN mice than in BALB/c mice. Therefore, gamma delta TCR+ T cells are partly responsible for the expression of host resistance against the MAC in the early phase of infection. However, the subsequent decrease in the level of gamma delta TCR+ T cells was observed by week 5. Thus, in the case of chronic state of MAC infection, the size of gamma delta TCR+ T cell-pool seems to be in normal level. This suggests that per cell activity of gamma delta TCR+ T cells rather than mobilizing number of them is important factor in the mechanisms for occurrence of allergic diseases including Behçet disease. Although, the early increase in gamma delta TCR+ T cells of peritoneal cells was also observed during the course of M. fortuitum infection, the degree of induction of gamma delta TCR+ T cells in A/J mice (M. fortuitum-susceptible) was in similar level as that in BALB/c mice (M. fortuitum-resistant).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

为了解鸟分枝杆菌复合体(MAC)感染诱导的γδTCR⁺T细胞参与宿主抵抗力表达及白塞病发生的可能性,我们检测了它们在MAC感染的宿主小鼠中的行为。在BALB/c(Bcgs;对MAC易感)和CBA/JN(Bcgr;对MAC有抵抗力)品系小鼠中,经腹腔内途径感染胞内分枝杆菌后第1至2周左右,宿主腹腔淋巴细胞中γδTCR⁺T细胞数量出现短暂但明显的增加。γδTCR⁺T细胞的诱导程度在CBA/JN小鼠中略高于BALB/c小鼠。因此,γδTCR⁺T细胞在感染早期部分负责宿主对MAC抵抗力的表达。然而,到第5周时观察到γδTCR⁺T细胞水平随后下降。因此,在MAC感染的慢性状态下,γδTCR⁺T细胞库的大小似乎处于正常水平。这表明γδTCR⁺T细胞的单细胞活性而非其动员数量是包括白塞病在内的过敏性疾病发生机制中的重要因素。虽然在偶然分枝杆菌感染过程中也观察到腹腔细胞中γδTCR⁺T细胞的早期增加,但A/J小鼠(对偶然分枝杆菌易感)中γδTCR⁺T细胞的诱导程度与BALB/c小鼠(对偶然分枝杆菌有抵抗力)中的相似。(摘要截短于250字)

相似文献

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[Behaviour of gamma delta TCR+ T cells during the course of nontuberculous mycobacterial infections and proliferative response of host lymphocytes to 65kD heat shock protein].[非结核分枝杆菌感染过程中γδTCR + T细胞的行为及宿主淋巴细胞对65kD热休克蛋白的增殖反应]
Kekkaku. 1993 Feb;68(2):99-104.
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Heat shock protein 65 induced by gammadelta T cells prevents apoptosis of macrophages and contributes to host defense in mice infected with Toxoplasma gondii.γδT细胞诱导的热休克蛋白65可防止巨噬细胞凋亡,并有助于感染弓形虫的小鼠的宿主防御。
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Gamma delta T cells play an important role in hsp65 expression and in acquiring protective immune responses against infection with Toxoplasma gondii.γδ T细胞在热休克蛋白65(HSP65)表达以及获得针对弓形虫感染的保护性免疫反应中发挥重要作用。
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Gamma Delta (γδ) T Cells and Their Involvement in Behçet's Disease.γδ T 细胞及其在贝赫切特病中的作用。
J Immunol Res. 2015;2015:705831. doi: 10.1155/2015/705831. Epub 2015 Oct 11.