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TNF Receptor-Associated Factor 6-Dependent CD40 Signaling Primes Macrophages to Acquire Antimicrobial Activity in Response to TNF-¹

Rosa M. Andrade^*, Matthew Wessendarp^*, Jose-Andres C. Portillo^*, Jun-Qi Yang^*, Francisco J. Gomez^*, Joan E. Durbin, Gail A. Bishop and Carlos S. Subauste^2,*

^* Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267; Children’s Research Institute, The Ohio State University College of Medicine and Public Health, Columbus, OH 43205; and Department of Microbiology, University of Iowa and Veterans Affairs Medical Center, Iowa City, IA 52242

IFN- is considered an essential stimulus that allows macrophages to acquire activity against intracellular pathogens in response to a second signal such as TNF-. However, protection against important pathogens can take place in the absence of IFN- through mechanisms that are still dependent on TNF-. Engagement of CD40 modulates antimicrobial activity in macrophages. However, it is not known whether CD40 can replace IFN- as priming signal for induction of this response. We show that CD40 primes mouse macrophages to acquire antimicrobial activity in response to TNF-. The effect of CD40 was not caused by modulation of IL-10 and TGF- production or TNFR expression and did not require IFN- signaling. Induction of antimicrobial activity required cooperation between TNFR-associated factor 6-dependent CD40 signaling and TNFR2. These results support a paradigm where TNFR-associated factor 6 signaling downstream of CD40 alters the pattern of response of macrophages to TNF- leading to induction of antimicrobial activity.

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