| First Author | Overstreet MG | Year | 2013 |
| Journal | Nat Immunol | Volume | 14 |
| Issue | 9 | Pages | 949-58 |
| PubMed ID | 23933892 | Mgi Jnum | J:208230 |
| Mgi Id | MGI:5562506 | Doi | 10.1038/ni.2682 |
| Citation | Overstreet MG, et al. (2013) Inflammation-induced interstitial migration of effector CD4(+) T cells is dependent on integrin alphaV. Nat Immunol 14(9):949-58 |
| abstractText | Leukocytes must traverse inflamed tissues to effectively control local infection. Although motility in dense tissues seems to be integrin independent and based on actomyosin-mediated protrusion and contraction, during inflammation, changes to the extracellular matrix (ECM) may necessitate distinct motility requirements. Indeed, we found that the interstitial motility of T cells was critically dependent on Arg-Gly-Asp (RGD)-binding integrins in the inflamed dermis. Inflammation-induced deposition of fibronectin was functionally linked to higher expression of integrin alphaV on effector CD4(+) T cells. By intravital multiphoton imaging, we found that the motility of CD4(+) T cells was dependent on alphaV expression. Selective blockade or knockdown of alphaV arrested T helper type 1 (TH1) cells in the inflamed tissue and attenuated local effector function. Our data demonstrate context-dependent specificity of lymphocyte movement in inflamed tissues that is essential for protective immunity. |
