| First Author | Byeseda SE | Year | 2009 |
| Journal | Am J Pathol | Volume | 175 |
| Issue | 2 | Pages | 571-9 |
| PubMed ID | 19608878 | Mgi Jnum | J:150953 |
| Mgi Id | MGI:3852583 | Doi | 10.2353/ajpath.2009.090112 |
| Citation | Byeseda SE, et al. (2009) ICAM-1 is necessary for epithelial recruitment of gammadelta T cells and efficient corneal wound healing. Am J Pathol 175(2):571-9 |
| abstractText | Wound healing and inflammation are both significantly reduced in mice that lack gammadelta T cells. Here, the role of epithelial intercellular adhesion molecule-1 (ICAM-1) in gammadelta T cell migration in corneal wound healing was assessed. Wild-type mice had an approximate fivefold increase in epithelial gammadelta T cells at 24 hours after epithelial abrasion. ICAM-1(-/-) mice had 50.9% (P < 0.01) fewer gammadelta T cells resident in unwounded corneal epithelium, which failed to increase in response to epithelial abrasion. Anti-ICAM-1 blocking antibody in wild-type mice reduced epithelial gammadelta T cells to a number comparable to that of ICAM-1(-/-) mice, and mice deficient in lymphocyte function-associated antigen-1 (CD11a/CD18), a principal leukocyte receptor for ICAM-1, exhibited a 48% reduction (P < 0.01) in peak epithelial gammadelta T cells. Re-epithelialization and epithelial cell division were both significantly reduced ( approximately 50% at 18 hours, P < 0.01) after abrasion in ICAM-1(-/-) mice versus wild-type, and at 96 hours, recovery of epithelial thickness was only 66% (P < 0.01) of wild-type. ICAM-1 expression by corneal epithelium in response to epithelial abrasion appears to be critical for accumulation of gammadelta T cells in the epithelium, and deficiency of ICAM-1 significantly delays wound healing. Since gammadelta T cells are necessary for efficient epithelial wound healing, ICAM-1 may contribute to wound healing by facilitating gammadelta T cell migration into the corneal epithelium. |
