ArticleRespiratory research2025
TLR5 activation in respiratory epithelial cells orchestrate mucosal Th17 response through both indirect and direct pathways.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundFlagellin, a potent mucosal adjuvant administered via the intranasal route, has been widely recognized for its capacity to enhance immune responses against diverse pathogens. However, the effects and the underlying mechanisms by which flagellin modulates CD4
methodsRecombinant flagellin proteins, including full-length flagellin (SF) and a TLR5-binding deficient variant (SFΔ90-97), were produced and purified. An OT-II derived CD4
resultsFlagellin preferentially promotes Th17 cells differentiation. Respiratory epithelial cells (RECs), acting as sentinel cells, are the first to encounter exogenous stimuli during intranasal immunization. Flagellin stimulates the secretion of various soluble cytokines by binding to TLR5 on the surface of RECs, with GM-CSF facilitating the functional activation of airway DCs. GM-CSF-conditioned DCs exhibit upregulated IL-6 expression which in turn drives the polarization of naïve CD4
conclusionFlagellin preferentially induced a Th17-enhanced immune response and RECs were highlighted its essential roles during this process through both indirect and direct pathways. For indirect pathway, RECs modulate DC function through GM-CSF. Moreover, RECs directly contribute to Th17 differentiation by secreting IL-6.
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