CD4+ T-cell population mediates development of inflammatory bowel disease in T-cell receptor alpha chain-deficient mice.
CD4+ T-cell population mediates development of inflammatory bowel disease in T-cell receptor alpha chain-deficient mice.
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DOI：
10.1053/gast.1997.v112.pm9178680
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发表时间：
1997-06
期刊：
影响因子：
29.4
通讯作者：
I. Takahashi;Hiroshi Kiyono;Shigeyuki Hamada
中科院分区：
文献类型：
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作者：
I. Takahashi;Hiroshi Kiyono;Shigeyuki Hamada
背景与目的在患有炎症性肠病（IBD）的TCR α-/-小鼠的粘膜和外周淋巴组织中观察到表达CD 4和T细胞受体（TCR）α-β +（β [dim]）的T细胞增加。本研究的目的是表征CD 4 + TCR α-β + T细胞。方法检测CD 4 + TCR α-β + T细胞的细胞因子产生、TCR V β的使用和派尔集合淋巴结B细胞的辅助功能。结果从IBD小鼠肠系膜淋巴结和肠道固有层中纯化的CD 4 + TCR α-β + T细胞仅产生IL 4，使用选定的TCR亚群（V β 6，V β 8，V β 14和V β 15），并在葡萄球菌肠毒素B刺激后大量增殖。将CD 4 + TCR α-β + T细胞添加到派尔集合淋巴结B细胞培养物中显著增强免疫球蛋白（IG）A、IgG和IgM抗体应答。此外，用抗TCR β链的单克隆抗体消耗TCR α-β + T细胞完全抑制了TCR α-/-小鼠中IBD和多克隆B细胞活化的发作。结论TCR α-/-小鼠IBD的发生与CD 4 + TCR α-β + T细胞介导有关。
BACKGROUND & AIMS Increase of T cells expressing CD4 and T-cell receptor (TCR) alpha- beta+ (beta[dim]) was observed in the mucosal and peripheral lymphoid tissues of TCR alpha-/- mice with inflammatory bowel disease (IBD). The aim of this study was to characterize the CD4+ TCR alpha-beta+ T cells. METHODS Cytokine production, TCR V beta usage, and helper function for Peyer's patch B cells by the CD4+ TCR alpha-beta+ T cells were assessed. RESULTS The CD4+ TCR alpha-beta+ T cells purified from mesenteric lymph nodes and lamina propria of the intestine of IBD mice exclusively produced interleukin 4, used selected subsets (V beta6, V beta8, V beta14, and V beta15) of TCR, and massively proliferated after stimulation with staphylococcal enterotoxin B. Addition of the CD4+ TCR alpha-beta+ T cells to Peyer's patch B-cell cultures markedly enhanced immunoglobulin (Ig) A, IgG, and IgM antibody responses. Furthermore, depletion of the TCR alpha-beta+ T cells with monoclonal antibody against TCR beta chain completely suppressed the onset of IBD and polyclonal B-cell activation in the TCR alpha-/- mice. CONCLUSIONS These findings suggest the CD4+ TCR alpha-beta+ T cells-mediated development of IBD in TCR alpha-/- mice.