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*Substance via MeSH
The Journal of Immunology, 2001, 166: 270-276.
Copyright © 2001 by The American Association of Immunologists

Enhanced Secretion of IFN-{gamma} by Activated Th1 Cells Occurs Via Reverse Signaling Through TNF-Related Activation-Induced Cytokine1

Nien-Jung Chen*, Mei-Wen Huang* and Shie-Liang Hsieh2,*,{dagger}

* Department of Microbiology and Immunology, and {dagger} Immunology Research Center, National Yang-Ming University, Taipei, Taiwan

Growing evidence has demonstrated that members of TNF superfamily transduce signals after engagement with their receptors. TNF-related activation-induced cytokine (TRANCE), a member of TNF superfamily, is preferentially expressed on the surface of activated CD4+ Th1 cells. The soluble receptor activator of NF-{kappa}B (RANK).Fc fusion protein suppresses IFN-{gamma} secretion by activated Th1 cells, but does not affect IL-4 secretion by Th2 cells. The suppressive effect on IFN-{gamma} secretion is observed when Th1 cells are activated by APCs, but not by immobilized anti-TCR{beta} mAb. In contrast, immobilized RANK.Fc fusion protein augments IFN-{gamma} secretion by Th1 cells, indicating the occurrence of reverse signaling through TRANCE during T cell/APC interaction. The enhanced secretion of IFN-{gamma} mediated via TRANCE correlates with the activation of p38 mitogen-activated protein kinase and is blocked by SB203580, a p38 mitogen-activated protein kinase-specific inhibitor. Thus, in addition to its role in activating dendritic cells by binding to the receptor RANK, TRANCE itself can signal the augmentation of IFN-{gamma} secretion via a p38-dependent pathway, and this provides yet another example of reverse signaling by a member of TNF superfamily.




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