|
|
|
|
|
|
|
||
J. Exp. Med.,
Volume 187, Number 3, February 2, 1998 307-317
By
From the * Microbiology Section, Department of Experimental Medicine and Biochemical Sciences,
University of Perugia, 06122 Perugia, Italy; and 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)- The Basel Institute for Immunology, CH-L005
Basel, Switzerland
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- 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.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
