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Updated: Aug 15, 2026

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
Published on: April 16, 2015
c-Rel-dependent priming of naive T cells by inflammatory cytokines
Daliya Banerjee1, Hsiou-Chi Liou, Ranjan Sen
1Rosenstiel Research Center and Department of Biology, Brandeis University, Waltham, Massachusetts 02454, USA.
Abstract:
The intrinsic refractoriness of naive T cells for cytokine production is counteracted by cells of the innate immune system. Upon sensing danger via Toll-like receptors, these cells upregulate T cell costimulatory molecules and secrete cytokines that enhance T cell activation. We show that cytokine-mediated priming of naive T cells requires the NF-kappaB family member c-Rel. In resting naive cells c-Rel is associated primarily with IkappaBbeta, an inhibitory molecule that is not effectively degraded by TCR signals. Exposure of T cells to proinflammatory cytokines, TNF-alpha and IL-1beta, shifts c-Rel to IkappaBalpha-associated complexes that are readily targeted by the TCR. As a consequence, IL-2 and IFN-gamma mRNA are produced more quickly, and at higher levels, in cytokine-primed T cells. This mechanism does not operate in effector T cells where cytokine gene expression is c-Rel-independent. We propose that c-Rel plays a crucial role as a target of innate signals in T cells.
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