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CD154 Activates Macrophage Antimicrobial Activity in the Absence of IFN- through a TNF--Dependent Mechanism ¹

Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267

Protection against certain intracellular pathogens can take place in the absence of IFN- through mechanisms dependent on TNF-. In this regard, patients with partial defect in IFN- receptor 1 are not susceptible to toxoplasmosis. Thus, we used a model of Toxoplasma gondii infection to investigate whether CD154 modulates IFN--independent mechanisms of host protection. Human monocyte-derived macrophages treated with recombinant CD154 exhibited increased anti-T. gondii activity. The number of tachyzoites per 100 macrophages at 20 h postinfection was lower in CD154-treated macrophages compared with controls. This was accompanied by a decrease in the percentage of infected cells in CD154-treated macrophages at 20 h compared with 1 h postinfection. CD154-bearing cells also induced antimicrobial activity in T. gondii-infected macrophages. CD154 enhanced macrophage anti-T. gondii activity independently of IFN-. TNF- mediated the effects of CD154 on macrophage anti-T. gondii activity. CD154 increased TNF- production by T. gondii-infected macrophages, and neutralization of TNF- inhibited the effect of CD154 on macrophage anti-T. gondii activity. These results demonstrate that CD154 triggers TNF--dependent antimicrobial activity in macrophages and suggest that CD154 regulates the mechanisms of host protection that take place when IFN- signaling is deficient.

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