Overstreet, Michael G.Gaylo, AlisonAngermann, BastianHughson, AngelaHyun, Young-minLambert, KrisAcharya, MriduBillroth-Maclurg, Alison C.Rosenberg, Alexander F.Topham, David J.Yagita, HideoKim, MinsooLacy-Hulbert, AdamMeier-Schellersheim, MartinFowell, Deborah J.2014-10-012014Overstreet, M. G., A. Gaylo, B. Angermann, A. Hughson, Y. Hyun, K. Lambert, M. Acharya, et al. 2014. “Inflammation-induced effector CD4+ T cell interstitial migration is alpha-v integrin dependent.” Nature immunology 14 (9): 949-958. doi:10.1038/ni.2682. http://dx.doi.org/10.1038/ni.2682.1529-2908http://nrs.harvard.edu/urn-3:HUL.InstRepos:12987318Leukocytes must traverse inflamed tissues to effectively control local infection. Although motility in dense tissues appears to be integrin-independent actin-myosin based, during inflammation changes to the extracellular matrix (ECM) may necessitate distinct motility requirements. Indeed, we found that T cell interstitial motility was critically dependent on RGD-binding integrins in the inflamed dermis. Inflammation-induced deposition of fibronectin was functionally linked to increased αv integrin expression on effector CD4+ T cells. Using intravital multi-photon imaging, we found that CD4+ T cell motility was dependent on αv expression. Selective αv blockade or knockdown arrested TH1 motility in the inflamed tissue and attenuated local effector function. These data show a context-dependent specificity of lymphocyte movement in inflamed tissues that is essential for protective immunity.en-USJournal Article2014-10-0110.1038/ni.2682