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Laminins affect T cell trafficking and allograft fate

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タイトル: Laminins affect T cell trafficking and allograft fate
著者: Warren, Kristi J. 著作を一覧する
Iwami, Daiki 著作を一覧する
Harris, Donald G. 著作を一覧する
Bromberg, Jonathan S. 著作を一覧する
Burrell, Bryna E. 著作を一覧する
発行日: 2014年 5月 1日
出版者: American Society for Clinical Investigation
誌名: The Journal of clinical investigation
巻: 124
号: 5
開始ページ: 2204
終了ページ: 2218
出版社 DOI: 10.1172/JCI73683
抄録: Lymph nodes (LNs) are integral sites for the generation of immune tolerance, migration of CD4+ T cells, and induction of Tregs. Despite the importance of LNs in regulation of inflammatory responses, the LN-specific factors that regulate T cell migration and the precise LN structural domains in which differentiation occurs remain undefined. Using intravital and fluorescent microscopy, we found that alloreactive T cells traffic distinctly into the tolerant LN and colocalize in exclusive regions with alloantigen-presenting cells, a process required for Treg induction. Extracellular matrix proteins, including those of the laminin family, formed regions within the LN that were permissive for colocalization of alloantigen-presenting cells, alloreactive T cells, and Tregs. We identified unique expression patterns of laminin proteins in high endothelial venule basement membranes and the cortical ridge that correlated with alloantigen-specific immunity or immune tolerance. The ratio of laminin α4 to laminin α5 was greater in domains within tolerant LNs, compared with immune LNs, and blocking laminin α4 function or inducing laminin α5 overexpression disrupted T cell and DC localization and transmigration through tolerant LNs. Furthermore, reducing α4 laminin circumvented tolerance induction and induced cardiac allograft inflammation and rejection in murine models. This work identifies laminins as potential targets for immune modulation.
資料タイプ: article
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 岩見 大基


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