Gene interactions and pathways from curated databases and text-mining

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ICOS — TNF

Text-mined interactions from Literome

Gonzalo et al., J Immunol 2001 : ICOS-Ig , but not CTLA4-Ig, uniquely regulates SAg induced TNF-alpha production, whereas IL-2 secretion is modulated by CTLA4-Ig, but not ICOS-Ig ... Our data suggest that ICOS and CD28 regulate T cell expansion and that ligation of either CD28 or ICOS can either uniquely regulate cytokine production ( IL-2/TNF-alpha ) or synergize for optimal cytokine production ( IL-4 ) after SAg administration
Scales et al., Eur J Immunol 2004 (Helminthiasis, Animal...) : We show that, although blocking ICOS resulted in a decrease in TNF-alpha and the Th2 cytokines IL-4 and IL-5 and serum levels of total IgE, it did not affect the expulsion of the adult parasites
Nakae et al., J Immunol 2006 : We found that IgE- and Ag-dependent mast cell enhancement of T cell activation required secreted TNF ; that TNF can increase the surface expression of OX40, ICOS , PD-1, and other costimulatory molecules on CD3 ( + ) T cells ; and that a neutralizing Ab to OX40L, but not neutralizing Abs to ICOSL or PD-L1, significantly reduced IgE/Ag dependent mast cell mediated enhancement of T cell activation
Mesturini et al., Eur J Immunol 2006 : ICOS strikingly potentiated secretion of IL-2, IFN-gamma, IL-10, and TNF-alpha , but not IL-4, promoted by optimal stimulation of CD3+CD28, and it was the key switching-factor of activation when cells received suboptimal stimulation of CD3+CD28 or stimulation of CD3 alone in the presence of exogenous IL-2
Usui et al., Invest Ophthalmol Vis Sci 2010 (Behcet Syndrome...) : High ICOS expression in BD patients with uveitis contributed to the upregulation of IFN-?, IL-17, and TNF-a production, suggesting that abnormal ICOS costimulation may play an immunopathologic role in the pathogenesis of uveitis in BD
Ogata et al., Int Immunol 2013 : We also showed that pDC derived TNF-a induced ICOS-L expression on pDCs in an autocrine manner and that IL-6 promoted ICOS expression on T-cells, contributing to the ICOS/ICOS-L mediated T-cell response