| First Author | Mrass P | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Issue | 1 | Pages | 1010 |
| PubMed ID | 29044117 | Mgi Jnum | J:347485 |
| Mgi Id | MGI:6100848 | Doi | 10.1038/s41467-017-01032-2 |
| Citation | Mrass P, et al. (2017) ROCK regulates the intermittent mode of interstitial T cell migration in inflamed lungs. Nat Commun 8(1):1010 |
| abstractText | Effector T cell migration through tissues can enable control of infection or mediate inflammatory damage. Nevertheless, the molecular mechanisms that regulate migration of effector T cells within the interstitial space of inflamed lungs are incompletely understood. Here, we show T cell migration in a mouse model of acute lung injury with two-photon imaging of intact lung tissue. Computational analysis indicates that T cells migrate with an intermittent mode, switching between confined and almost straight migration, guided by lung-associated vasculature. Rho-associated protein kinase (ROCK) is required for both high-speed migration and straight motion. By contrast, inhibition of Galphai signaling with pertussis toxin affects speed but not the intermittent migration of lung-infiltrating T cells. Computational modeling shows that an intermittent migration pattern balances both search area and the duration of contacts between T cells and target cells. These data identify that ROCK-dependent intermittent T cell migration regulates tissue-sampling during acute lung injury. |
