Journal
SCIENCE SIGNALING
Volume 12, Issue 577, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scisignal.aar3641
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Funding
- Consejo Nacional de Ciencia y Tecnologia (CONACYT) [253310]
- CONACYT [168182, 257188]
- Programa de Mejoramiento del Profesorado (PROMEPSI) [UAEM/13/342]
- French Plan Cancer in the context of the project CoMET (2014-2017)
- French Agence Nationale pour la Recherche
- SEP-CONACYT-ANUIES-ECOS NORD [M11S01, M17S02]
- French Plan Cancer in the context of the project SYSTAIM (2015-2019)
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CD4(+) T cells recognize antigens through their T cell receptors (TCRs); however, additional signals involving costimulatory receptors, for example, CD28, are required for proper T cell activation. Alternative costimulatory receptors have been proposed, including members of the Toll-like receptor (TLR) family, such as TLR5 and TLR2. To understand the molecular mechanism underlying a potential costimulatory role for TLR5, we generated detailed molecular maps and logical models for the TCR and TLR5 signaling pathways and a merged model for cross-interactions between the two pathways. Furthermore, we validated the resulting model by analyzing how T cells responded to the activation of these pathways alone or in combination, in terms of the activation of the transcriptional regulators CREB, AP-1 (c-Jun), and NF-kappa B (p65). Our merged model accurately predicted the experimental results, showing that the activation of TLR5 can play a similar role to that of CD28 activation with respect to AP-1, CREB, and NF-kappa B activation, thereby providing insights regarding the cross-regulation of these pathways in CD4(+) T cells.
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