| First Author | Mencacci A | Year | 1998 |
| Journal | J Immunol | Volume | 161 |
| Issue | 11 | Pages | 6228-37 |
| PubMed ID | 9834110 | Mgi Jnum | J:115101 |
| Mgi Id | MGI:3690671 | Doi | 10.4049/jimmunol.161.11.6228 |
| Citation | Mencacci A, et al. (1998) IL-10 is required for development of protective Th1 responses in IL-12-deficient mice upon Candida albicans infection. J Immunol 161(11):6228-37 |
| abstractText | IL-12 is both required and prognostic for Th1 development in mice with Candida albicans infection. To delineate further the physiologic role of IL-12 in antifungal immunity, mice deficient for this cytokine were assessed for susceptibility to C. albicans infections, and for parameters of innate and adaptive immunity. IL-12-deficient mice were highly susceptible to gastrointestinal infection or to reinfection and showed elevated production of Candida-specific IgE and IL-4 and defective production of IFN-gamma. The failure to mount protective Th1 responses occurred despite the presence of an unimpaired innate antifungal immune response, which correlated with unaltered IFN-gamma production, but defective production of, and responsiveness to, inhibitory IL-10. IL-10 or IL-12 neutralization increased the innate antifungal resistance in wild-type mice. However, in IL-12-deficient mice, treatment with exogenous IL-12 or IL-10 impaired IL-4 production and increased resistance to infection, through a negative effect on the CTLA-4/B7-2 costimulatory pathway. These results confirm the obligatory role of IL-12 in the induction of anticandidal Th1 responses, and indicate the existence of a positive regulatory loop between IL-12 and IL-10 that may adversely affect the innate antifungal response, but is required for optimal costimulation of IL-12-dependent CD4+ Th1 cells. |
