| First Author | Witherden DA | Year | 2012 |
| Journal | Immunity | Volume | 37 |
| Issue | 2 | Pages | 314-25 |
| PubMed ID | 22902232 | Mgi Jnum | J:187369 |
| Mgi Id | MGI:5436328 | Doi | 10.1016/j.immuni.2012.05.026 |
| Citation | Witherden DA, et al. (2012) The CD100 Receptor Interacts with Its Plexin B2 Ligand to Regulate Epidermal gammadelta T Cell Function. Immunity 37(2):314-25 |
| abstractText | gammadelta T cells respond rapidly to keratinocyte damage, providing essential contributions to the skin wound healing process. The molecular interactions regulating their response are unknown. Here, we identify a role for interaction of plexin B2 with the CD100 receptor in epithelial repair. In vitro blocking of plexin B2 or CD100 inhibited gammadelta T cell activation. Furthermore, CD100 deficiency in vivo resulted in delayed repair of cutaneous wounds due to a disrupted gammadelta T cell response to keratinocyte damage. Ligation of CD100 in gammadelta T cells induced cellular rounding via signals through ERK kinase and cofilin. Defects in this rounding process were evident in the absence of CD100-mediated signals, thereby providing a mechanistic explanation for the defective wound healing in CD100-deficient animals. The discovery of immune functions for plexin B2 and CD100 provides insight into the complex cell-cell interactions between epithelial resident gammadelta T cells and the neighboring cells they support. |
