| First Author | Mencacci A | Year | 1998 |
| Journal | J Exp Med | Volume | 187 |
| Issue | 3 | Pages | 307-17 |
| PubMed ID | 9449711 | Mgi Jnum | J:111437 |
| Mgi Id | MGI:3653990 | Doi | 10.1084/jem.187.3.307 |
| Citation | Mencacci A, et al. (1998) Endogenous interleukin 4 is required for development of protective CD4+ T helper type 1 cell responses to Candida albicans. J Exp Med 187(3):307-17 |
| abstractText | Interleukin (IL)-4-deficient mice were used to assess susceptibility to systemic or gastrointestinal Candida albicans infections, as well as parameters of innate and elicited T helper immunity. In the early stage of systemic infection with virulent C. albicans, an unopposed interferon (IFN)-gamma response renders IL-4-deficient mice more resistant than wild-type mice to infection. Yet, IL-4-deficient mice failed to efficiently control infection in the late stage and succumbed to it. Defective IFN-gamma and IL-12 production, but not IL-12 responsiveness, was observed in IL-4-deficient mice that failed to mount protective T helper type 1 cell (Th1)-mediated acquired immunity in response to a live vaccine strain of the yeast or upon mucosal immunization in vivo. In vitro, IL-4 primed neutrophils for cytokine release, including IL-12. However, late treatment with exogenous IL-4, while improving the outcome of infection, potentiated CD4(+) Th1 responses even in the absence of neutrophils. These findings indicate that endogenous IL-4 is required for the induction of CD4(+) Th1 protective antifungal responses, possibly through the combined activity on cells of the innate and adaptive immune systems. |
