| First Author | Cunnusamy K | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 8 | Pages | 4651-8 |
| PubMed ID | 20844197 | Mgi Jnum | J:164882 |
| Mgi Id | MGI:4835588 | Doi | 10.4049/jimmunol.1001576 |
| Citation | Cunnusamy K, et al. (2010) IL-17 promotes immune privilege of corneal allografts. J Immunol 185(8):4651-8 |
| abstractText | Corneal allograft rejection has been described as a Th1-mediated process involving IFN-gamma production. However, it has been reported that corneal allograft rejection soars in IFN-gamma(-/-) mice or mice treated with anti-IFN-gamma mAb. Th17 is a recently described IL-17A-producing Th cell population that has been linked to renal and cardiac graft rejection, which was originally thought to be Th1-mediated. We tested the hypothesis that Th17 cells mediate corneal allograft rejection in an IL-17A-dependent fashion and unexpectedly found that depletion of IL-17A increased the incidence of rejection to 90%. We demonstrate that the exacerbated rejection following depletion of IL-17A did not result from a loss of cross-regulation of Th1 cells or exaggerated delayed-type hypersensitivity responses. Instead, inhibition of the Th1 or Th17 cell lineages promoted the emergence of a Th2 cell subset that independently mediated allograft rejection. These findings demonstrate that IL-17A is not required for corneal allograft rejection and may instead contribute to the immune privilege of corneal allografts. |
