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首页> 外文期刊>Journal of interferon and cytokine research: The official journal of the International Society for Interferon and Cytokine Research >CXCL10-producing mucosal CD4+ T cells, NK cells, and NKT cells are associated with chronic colitis in IL-10(-/-) mice, which can be abrogated by anti-CXCL10 antibody inhibition.
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CXCL10-producing mucosal CD4+ T cells, NK cells, and NKT cells are associated with chronic colitis in IL-10(-/-) mice, which can be abrogated by anti-CXCL10 antibody inhibition.

机译：产生CXCL10的粘膜CD4 + T细胞，NK细胞和NKT细胞与IL-10（-/-）小鼠中的慢性结肠炎有关，可以通过抗CXCL10抗体抑制来消除这种慢性结肠炎。

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We have shown previously that there is a temporal increase in the levels of CXCL10 and CXCR3 mRNA during spontaneous murine colitis. We now show that CXCL10 is significantly expressed by mucosal CD4+ T cells, natural killer (NK) cells, and NKT cells, but not by dendritic cells (DCs), during chronic murine colitis. CXCL10 blockade alleviated chronic colitis and attenuated the associated increase in serum amyloid A (SAA), interleukin-12 (IL-12)p40, tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), IL-1 alpha, and IL-1 beta levels as well as in the number of CD4+ T, NKT, and NK cells that express CXCL10 and CXCR3, compared with groups treated with control antibody (Ab). After CXCL10 blockade, the number of CXCR3+ DCs in the mesenteric lymph nodes (MLNs) and Peyer's patches (PPs) were increased to levels found before the onset of colitis. In contrast, the numbers of splenic and intestinal lamina propria (LP) CXCR3+ DCs were reduced after anti-CXCL10 Ab treatment, compared with controls. Ex vivo antigen and CXCL10 stimulation of mucosal cells caused an increase in MHC class II, CD40, and CD86 as well as a decrease in CD30 ligand (CD30L) expression by DCs. This study provides insights into CXCL10 expression during inflammatory bowel disease (IBD) and the cellular and molecular mechanisms of CXCL10-mediated colitis. Our data also support the premise that CXCL10 blockade can attenuate chronic colitis by preventing the activation and recruitment of CXCR3+ leukocytes during IBD.
机译：先前我们已经显示，自发鼠科结肠炎期间CXCL10和CXCR3 mRNA的水平随时间增加。我们现在显示，在慢性鼠结肠炎中，CXCL10由粘膜CD4 + T细胞，自然杀伤（NK）细胞和NKT细胞显着表达，而不由树突状细胞（DC）表达。 CXCL10阻滞缓解了慢性结肠炎，并减轻了血清淀粉样蛋白A（SAA），白介素12（IL-12）p40，肿瘤坏死因子-α（TNF-alpha），干扰素-γ（IFN-γ），IL-与用对照抗体（Ab）处理的组相比，表达CXCL10和CXCR3的CD1 +和IL-1 beta的水平以及CD4 + T，NKT和NK细胞的数量。在CXCL10阻滞后，肠系膜淋巴结（MLN）和Peyer斑块（PPs）中CXCR3 + DC的数量增加到结肠炎发作之前的水平。相反，与对照组相比，抗CXCL10 Ab治疗后脾和肠固有层（LP）CXCR3 + DC的数量减少了。粘膜细胞的离体抗原和CXCL10刺激导致DC引起II类MHC，CD40和CD86的增加以及CD30配体（CD30L）表达的减少。这项研究为炎症性肠病（IBD）期间CXCL10表达以及CXCL10介导的结肠炎的细胞和分子机制提供了见识。我们的数据还支持CXCL10阻断可以通过阻止IBD期间CXCR3 +白细胞的激活和募集而减轻慢性结肠炎的前提。

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