IFN-gamma is required for IL-12 responsiveness in mice with Candida albicans infection.
J Immunol
; 161(7): 3543-50, 1998 Oct 01.
Article
in En
| MEDLINE
| ID: mdl-9759875
ABSTRACT
To elucidate the role of IFN-gamma in antifungal CD4+ Th-dependent immunity, 129/Sv/Ev mice deficient for IFN-gamma receptor (IFN-gammaR(-/-)) were assessed for susceptibility to gastrointestinal or systemic Candida albicans infection and for parameters of innate and adaptive T helper immunity. IFN-gammaR(-/-) mice failed to mount protective Th1-mediated acquired immunity upon mucosal immunization or in response to a live vaccine strain of the yeast. The impaired Th1-mediated resistance correlated with defective IL-12 responsiveness, but not IL-12 production, and occurred in the presence of an increased innate antifungal resistance. The development of nonprotective Th2 responses was observed in IFN-gammaR(-/-) mice upon mucosal infection and subsequent reinfection. However, under experimental conditions of Th2 cell activation, the occurrence of Th2 cell responses was similar in IFN-gammaR(-/-) and in IFN-gammaR(+/+) mice. These results indicate the complex immunoregulatory role of IFN-gamma in the induction of mucosal and nonmucosal anticandidal Th cell responses; IFN-gamma is not essential for the occurrence of Th2 responses but is required for development of IL-12-dependent protective Th1-dependent immunity.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Candidiasis
/
Interferon-gamma
/
Interleukin-12
Limits:
Animals
Language:
En
Journal:
J Immunol
Year:
1998
Document type:
Article
Affiliation country:
Italy