IL-33 Increases the Magnitude of the Tissue-Resident Memory T Cell Response in Intestinal Tissues during Local Infection.

IF 3.6 3区 医学 Q2 IMMUNOLOGY Journal of immunology Pub Date : 2024-10-28 DOI:10.4049/jimmunol.2400323
Giuseppina Marchesini Tovar, Angie M Espinal, Corey Gallen, Tessa Bergsbaken
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Abstract

IL-33 plays an important role in the early programming of CD8 T cells; however, its contribution to the differentiation of tissue-resident memory T cells in vivo remains poorly defined. After infection of mice with Yersinia pseudotuberculosis, IL-33 expression was increased in the intestinal tissue, and this coincided with the expression of ST2 on T cells infiltrating the intestinal epithelium and lamina propria. Blocking IL-33 signaling after T cell infiltration of the intestinal tissue did not significantly impact the number or phenotype of tissue-resident memory T cells generated. However, overexpression of ST2 on T cells was able to increase expression of TCF1 and T cell number in the intestine compared with the lymphoid organs during infection. We also observed that enhanced accumulation and maintenance of ST2-overexpressing cells in the intestine postinfection were resolved. This points to a role for IL-33 in increasing the number of T cells that commit to intestinal tissue residency in vivo.

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IL-33 增加局部感染期间肠道组织中组织驻留记忆 T 细胞反应的幅度
IL-33 在 CD8 T 细胞的早期编程过程中发挥着重要作用;然而,它对体内组织驻留记忆 T 细胞分化的贡献仍未明确。小鼠感染耶尔森氏菌假结核病后,肠组织中 IL-33 的表达增加,这与浸润肠上皮和固有层的 T 细胞上 ST2 的表达相吻合。在 T 细胞浸润肠组织后阻断 IL-33 信号传导并不会显著影响所产生的组织驻留记忆 T 细胞的数量或表型。然而,与淋巴器官相比,在感染期间,T细胞上ST2的过表达能增加肠道中TCF1的表达和T细胞的数量。我们还观察到,感染后肠道中 ST2 表达细胞的增强积累和维持得到了解决。这表明,IL-33 在增加体内T细胞在肠道组织驻留的数量方面发挥了作用。
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来源期刊
Journal of immunology
Journal of immunology 医学-免疫学
CiteScore
8.20
自引率
2.30%
发文量
495
审稿时长
1 months
期刊介绍: The JI publishes novel, peer-reviewed findings in all areas of experimental immunology, including innate and adaptive immunity, inflammation, host defense, clinical immunology, autoimmunity and more. Special sections include Cutting Edge articles, Brief Reviews and Pillars of Immunology. The JI is published by The American Association of Immunologists (AAI)
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