Liz A Kurtz, Hope E Shearer, Rosanne Trevail, Menelaos Symeonides, Mobin Karimi, Nathan H Roy
{"title":"支架蛋白CasL抑制膜起泡,促进T细胞迁移。","authors":"Liz A Kurtz, Hope E Shearer, Rosanne Trevail, Menelaos Symeonides, Mobin Karimi, Nathan H Roy","doi":"10.1242/jcs.263792","DOIUrl":null,"url":null,"abstract":"<p><p>T cell migration into inflamed tissue is a key control point in the inflammatory response and relies on integrin interactions with their endothelial ligands. Here, we identify the signaling scaffold CasL (also known as Hef1 and NEDD9) as a central regulator of integrin-dependent migration in primary T cells. We found that CasL is specifically needed for efficient migration on ICAM-1-, but not VCAM-1-coated surfaces. Although wild-type T cells migrating on ICAM-1 formed an actin-rich cell front and move smoothly, T cells lacking CasL instead formed numerous, aberrant membrane blebs. CasL was needed for the normal distribution of F-actin in the cell front and phosphorylated myosin light chain in the cell rear, suggesting that CasL regulates the cytoskeletal architecture in migrating T cells. Importantly, using an in vivo allogeneic hematopoietic transplant model, we found that CasL promotes T cell migration into inflamed peripheral tissue, but was dispensable for trafficking to secondary lymphoid organs. Together, these results indicate CasL functions to control the balance of cytoskeletal components during integrin-dependent migration and highlight the importance of integrin signaling for proper migration into inflamed tissue.</p>","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3000,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The scaffold protein CasL restrains membrane blebbing and promotes T cell migration.\",\"authors\":\"Liz A Kurtz, Hope E Shearer, Rosanne Trevail, Menelaos Symeonides, Mobin Karimi, Nathan H Roy\",\"doi\":\"10.1242/jcs.263792\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>T cell migration into inflamed tissue is a key control point in the inflammatory response and relies on integrin interactions with their endothelial ligands. Here, we identify the signaling scaffold CasL (also known as Hef1 and NEDD9) as a central regulator of integrin-dependent migration in primary T cells. We found that CasL is specifically needed for efficient migration on ICAM-1-, but not VCAM-1-coated surfaces. Although wild-type T cells migrating on ICAM-1 formed an actin-rich cell front and move smoothly, T cells lacking CasL instead formed numerous, aberrant membrane blebs. CasL was needed for the normal distribution of F-actin in the cell front and phosphorylated myosin light chain in the cell rear, suggesting that CasL regulates the cytoskeletal architecture in migrating T cells. Importantly, using an in vivo allogeneic hematopoietic transplant model, we found that CasL promotes T cell migration into inflamed peripheral tissue, but was dispensable for trafficking to secondary lymphoid organs. Together, these results indicate CasL functions to control the balance of cytoskeletal components during integrin-dependent migration and highlight the importance of integrin signaling for proper migration into inflamed tissue.</p>\",\"PeriodicalId\":15227,\"journal\":{\"name\":\"Journal of cell science\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2025-07-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of cell science\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1242/jcs.263792\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/7/18 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cell science","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1242/jcs.263792","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/7/18 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
The scaffold protein CasL restrains membrane blebbing and promotes T cell migration.
T cell migration into inflamed tissue is a key control point in the inflammatory response and relies on integrin interactions with their endothelial ligands. Here, we identify the signaling scaffold CasL (also known as Hef1 and NEDD9) as a central regulator of integrin-dependent migration in primary T cells. We found that CasL is specifically needed for efficient migration on ICAM-1-, but not VCAM-1-coated surfaces. Although wild-type T cells migrating on ICAM-1 formed an actin-rich cell front and move smoothly, T cells lacking CasL instead formed numerous, aberrant membrane blebs. CasL was needed for the normal distribution of F-actin in the cell front and phosphorylated myosin light chain in the cell rear, suggesting that CasL regulates the cytoskeletal architecture in migrating T cells. Importantly, using an in vivo allogeneic hematopoietic transplant model, we found that CasL promotes T cell migration into inflamed peripheral tissue, but was dispensable for trafficking to secondary lymphoid organs. Together, these results indicate CasL functions to control the balance of cytoskeletal components during integrin-dependent migration and highlight the importance of integrin signaling for proper migration into inflamed tissue.