| First Author | Zhang H | Year | 2013 |
| Journal | Eur J Immunol | Volume | 43 |
| Issue | 10 | Pages | 2671-82 |
| PubMed ID | 23843112 | Mgi Jnum | J:201669 |
| Mgi Id | MGI:5515256 | Doi | 10.1002/eji.201242891 |
| Citation | Zhang H, et al. (2013) IL-17 plays a central role in initiating experimental Candida albicans infection in mouse corneas. Eur J Immunol 43(10):2671-82 |
| abstractText | The pathogenesis of fungal infection in the cornea remains largely unclear. To understand how the immune system influences the progression of fungal infection in corneas, we inoculated immunocompetent BALB/c mice, neutrophil- or CD4(+) T-cell-depleted BALB/c mice, and nude mice with Candida albicans. We found that only immunocompetent BALB/c mice developed typical Candida keratitis (CaK), while the other mouse strains lacked obvious clinical manifestations. Furthermore, CaK development was blocked in immunocompetent mice treated with anti-IL-17A or anti-IL-23p19 to neutralize IL-17 activity. However, no significant effects were observed when Treg cells, gammadelta T cells, or IFN-gamma were immunodepleted. Upon infection, the corneas of BALB/c mice were infiltrated with IL-17-producing leukocytes, including neutrophils and, to a lesser degree, CD4(+) T cells. In contrast, leukocyte recruitment to corneas was significantly diminished in nude mice. Indeed, nude mice produced much less chemokines (e.g. CXCL1, CXCL2, CXCL10, CXCL12, CCL2, and IL-6) in response to inoculation. Remarkably, addition of CXCL2 during inoculation restored CaK induction in nude mice. In contrast to its therapeutic effect on CaK, neutralization of IL-17 exacerbated Candida-induced dermatitis in skin. We conclude that IL-17, mainly produced by neutrophils and CD4(+) T cells in the corneas, is essential in the pathogenesis of CaK. |
