| First Author | Yamada D | Year | 2014 |
| Journal | J Immunol | Volume | 192 |
| Issue | 9 | Pages | 4112-21 |
| PubMed ID | 24670804 | Mgi Jnum | J:209980 |
| Mgi Id | MGI:5569199 | Doi | 10.4049/jimmunol.1300926 |
| Citation | Yamada D, et al. (2014) beta7 Integrin controls mast cell recruitment, whereas alphaE integrin modulates the number and function of CD8+ T cells in immune complex-mediated tissue injury. J Immunol 192(9):4112-21 |
| abstractText | Immune complex (IC) deposition causes significant tissue injury associated with various autoimmune diseases such as vasculitis. In the cascade of inflammation, cell-to-cell and cell-to-matrix adhesion via adhesion molecules are essential. To assess the role of alphaE and beta7 integrin in IC-mediated tissue injury, peritoneal and cutaneous reverse-passive Arthus reaction was examined in mice lacking alphaE integrin (alphaE(-/-)) or beta7 integrin (beta7(-/-)). Both alphaE(-/-) and beta7(-/-) mice exhibited significantly attenuated neutrophil infiltration in the peritoneal and cutaneous Arthus reaction. beta7 integrin deficiency, not alphaE integrin deficiency, significantly reduced the number of mast cells in the peritoneal cavity, which was consistent with the result that mast cells expressed only alpha4beta7 integrin, not alphaEbeta7 integrin. alphaE(-/-) mice instead revealed the reduction of CD8(+) T cells in the peritoneal cavity, and nearly half of them in wild-type mice expressed alphaE integrin. These alphaE(+)CD8(+) T cells produced more proinflammatory cytokines than alphaE(-)CD8(+) T cells, and adoptive transfer of alphaE(+)CD8(+) T cell into alphaE(-/-) recipients restored cutaneous and peritoneal Arthus reaction. These results suggest that in the peritoneal and cutaneous reverse-passive Arthus reaction, alpha4beta7 integrin is involved in the migration of mast cells for initial IC recognition. alphaEbeta7 integrin, in contrast, contributes by recruiting alphaE(+)CD8(+) T cells, which produce more proinflammatory cytokines than alphaE(-)CD8(+) T cells and amplify IC-mediated inflammation. |
