IL‐17 plays a central role in initiating experimental Candida albicans infection in mouse corneas

摘要: The pathogenesis of fungal infection in the cornea remains largely unclear. To understand how immune system influences progression corneas, we inoculated immunocompetent BALB/c mice, neutrophil- or CD4⁺ T-cell-depleted and nude mice with Candida albicans. We found that only developed typical keratitis (CaK), while other mouse strains lacked obvious clinical manifestations. Furthermore, CaK development was blocked treated anti-IL-17A anti-IL-23p19 to neutralize IL-17 activity. However, no significant effects were observed when Treg cells, γδ T IFN-γ immunodepleted. Upon infection, corneas infiltrated IL-17-producing leukocytes, including neutrophils and, a lesser degree, cells. In contrast, leukocyte recruitment significantly diminished mice. Indeed, produced much less chemokines (e.g. CXCL1, CXCL2, CXCL10, CXCL12, CCL2, IL-6) response inoculation. Remarkably, addition CXCL2 during inoculation restored induction contrast its therapeutic effect on CaK, neutralization exacerbated Candida-induced dermatitis skin. conclude IL-17, mainly by cells is essential CaK.