ICAM-1 Is Necessary for Epithelial Recruitment of {gamma}{delta} T Cells and Efficient Corneal Wound Healing

摘要

Wound healing and inflammation are both significantly reduced in mice that lack T cells. Here, the role of epithelial intercellular adhesion molecule-1 (ICAM-1) in T cell migration in corneal wound healing was assessed. Wild-type mice had an approximate fivefold increase in epithelial T cells at 24 hours after epithelial abrasion. ICAM-1–/– mice had 50.9% (P < 0.01) fewer 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 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 T cells. Re-epithelialization and epithelial cell division were both significantly reduced (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 T cells in the epithelium, and deficiency of ICAM-1 significantly delays wound healing. Since T cells are necessary for efficient epithelial wound healing, ICAM-1 may contribute to wound healing by facilitating T cell migration into the corneal epithelium.