Endogenous interleukin 4 is required for development of protective CD4+ T helper type 1 cell responses to Candida albicans.
Endogenous interleukin 4 is required for development of protective CD4+ T helper type 1 cell responses to Candida albicans.
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DOI：
10.1084/jem.187.3.307
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发表时间：
1998-02-02
期刊：
影响因子：
--
通讯作者：
Romani L
中科院分区：
文献类型：
--
作者：
Mencacci A;Del Sero G;Cenci E;d'Ostiani CF;Bacci A;Montagnoli C;Kopf M;Romani L
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)-γ 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-γ 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.
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影响因子：
2.2
作者：
LEZAMADAVILA, CM;WILLIAMS, DM;ALEXANDER, J
通讯作者：
ALEXANDER, J
DOI：
10.1084/jem.184.3.1127
发表时间：
1996-09-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Kopf M;Brombacher F;Köhler G;Kienzle G;Widmann KH;Lefrang K;Humborg C;Ledermann B;Solbach W
通讯作者：
Solbach W
影响因子：
6.4
作者：
PUCCETTI, P;MENCACCI, A;BISTONI, F
通讯作者：
BISTONI, F
影响因子：
5.4
作者：
Launois, P;Ohteki, T;Louis, JA
通讯作者：
Louis, JA
影响因子：
4.4
作者：
Pearce, EJ;Cheever, A;Kopf, M
通讯作者：
Kopf, M