{"title":"组织驻留辅助性 T 细胞的最佳维持需要持续的 B 细胞衍生 MHC II 类信号。","authors":"Young Min Son, In Su Cheon, Chaofan Li, Jie Sun","doi":"10.4049/immunohorizons.2300093","DOIUrl":null,"url":null,"abstract":"<p><p>Emerging studies have identified the critical roles of tissue-resident memory CD8+ T (TRM) and B (BRM) cells in the protection against mucosal viral infections, but the underlying mechanisms regulating robust development of TRM and BRM cells remain incompletely understood. We have recently shown that tissue-resident helper CD4+ T (TRH) cells, developed following influenza virus infection, function to sustain the optimal maintenance of TRM and BRM cells at the mucosal surface. In this study, we have explored the cellular and molecular cues modulating lung TRH persistence after influenza infection in C57BL/6 mice. We found that TRH cells were colocalized in tertiary lymphoid structures (TLSs) with local B cells. Abolishing TLSs or the depletion of B cells impaired lung TRH cell numbers. Of note, we found that persistent TCR signaling is needed for the maintenance of TRH cells after the clearance of infectious influenza virus. Furthermore, selective ablation of B cell-derived MHC class II resulted in partial reduction of lung TRH cell number after influenza infection. Our findings suggest that the interaction between lung-resident TRH cells and B cells, along with persistent Ag stimulation, is required to maintain TRH cells after respiratory viral infection.</p>","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"8 2","pages":"163-171"},"PeriodicalIF":0.0000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10916357/pdf/","citationCount":"0","resultStr":"{\"title\":\"Persistent B Cell-Derived MHC Class II Signaling Is Required for the Optimal Maintenance of Tissue-Resident Helper T Cells.\",\"authors\":\"Young Min Son, In Su Cheon, Chaofan Li, Jie Sun\",\"doi\":\"10.4049/immunohorizons.2300093\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Emerging studies have identified the critical roles of tissue-resident memory CD8+ T (TRM) and B (BRM) cells in the protection against mucosal viral infections, but the underlying mechanisms regulating robust development of TRM and BRM cells remain incompletely understood. We have recently shown that tissue-resident helper CD4+ T (TRH) cells, developed following influenza virus infection, function to sustain the optimal maintenance of TRM and BRM cells at the mucosal surface. In this study, we have explored the cellular and molecular cues modulating lung TRH persistence after influenza infection in C57BL/6 mice. We found that TRH cells were colocalized in tertiary lymphoid structures (TLSs) with local B cells. Abolishing TLSs or the depletion of B cells impaired lung TRH cell numbers. Of note, we found that persistent TCR signaling is needed for the maintenance of TRH cells after the clearance of infectious influenza virus. Furthermore, selective ablation of B cell-derived MHC class II resulted in partial reduction of lung TRH cell number after influenza infection. Our findings suggest that the interaction between lung-resident TRH cells and B cells, along with persistent Ag stimulation, is required to maintain TRH cells after respiratory viral infection.</p>\",\"PeriodicalId\":94037,\"journal\":{\"name\":\"ImmunoHorizons\",\"volume\":\"8 2\",\"pages\":\"163-171\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10916357/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ImmunoHorizons\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4049/immunohorizons.2300093\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ImmunoHorizons","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4049/immunohorizons.2300093","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
摘要
新近的研究发现,组织驻留记忆 CD8+ T 细胞(TRM)和 B 细胞(BRM)在抵御粘膜病毒感染方面发挥着关键作用,但人们对调控 TRM 和 BRM 细胞稳健发育的内在机制仍然知之甚少。我们最近的研究表明,流感病毒感染后形成的组织驻留辅助 CD4+ T(TRH)细胞具有维持粘膜表面 TRM 和 BRM 细胞最佳维持状态的功能。在这项研究中,我们探索了调节C57BL/6小鼠感染流感后肺部TRH持久性的细胞和分子线索。我们发现,TRH细胞与局部B细胞共定位在三级淋巴结构(TLS)中。消除三级淋巴结构或减少 B 细胞会影响肺 TRH 细胞的数量。值得注意的是,我们发现在传染性流感病毒清除后,TRH细胞的维持需要持续的TCR信号。此外,选择性消减B细胞衍生的MHC II类导致流感感染后肺TRH细胞数量部分减少。我们的研究结果表明,肺驻留的TRH细胞与B细胞之间的相互作用以及持续的Ag刺激是在呼吸道病毒感染后维持TRH细胞所必需的。
Persistent B Cell-Derived MHC Class II Signaling Is Required for the Optimal Maintenance of Tissue-Resident Helper T Cells.
Emerging studies have identified the critical roles of tissue-resident memory CD8+ T (TRM) and B (BRM) cells in the protection against mucosal viral infections, but the underlying mechanisms regulating robust development of TRM and BRM cells remain incompletely understood. We have recently shown that tissue-resident helper CD4+ T (TRH) cells, developed following influenza virus infection, function to sustain the optimal maintenance of TRM and BRM cells at the mucosal surface. In this study, we have explored the cellular and molecular cues modulating lung TRH persistence after influenza infection in C57BL/6 mice. We found that TRH cells were colocalized in tertiary lymphoid structures (TLSs) with local B cells. Abolishing TLSs or the depletion of B cells impaired lung TRH cell numbers. Of note, we found that persistent TCR signaling is needed for the maintenance of TRH cells after the clearance of infectious influenza virus. Furthermore, selective ablation of B cell-derived MHC class II resulted in partial reduction of lung TRH cell number after influenza infection. Our findings suggest that the interaction between lung-resident TRH cells and B cells, along with persistent Ag stimulation, is required to maintain TRH cells after respiratory viral infection.