ArticleFrontiers in cellular and infection microbiology2025
A TBC1D9-Rab29 axis controls homeostatic NF-κB signaling and selective IL-6 production in epithelial cells.
Article in Frontiers in cellular and infection microbiology, 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
Background: Interleukin-6 (IL-6) plays a crucial role in inflammation and immune defense; however, its intracellular trafficking and the mechanisms regulating its expression remain poorly understood. Methods: We investigated epithelial cell responses to poly(dA:dT) stimulation and group A Results: TBC1D9, a Rab GTPase-activating protein, selectively regulates IL-6: its depletion reduced IL-6 mRNA and protein levels without broadly affecting other pro-inflammatory cytokines. TBC1D9 maintained basal p65 phosphorylation but was dispensable for stimulus-induced NF-κB activation, supporting the idea that homeostatic NF-κB signaling is necessary for constitutive IL-6 transcription. Proteomics identified Rab29 as a TBC1D9 partner; co-immunoprecipitation showed preferential interaction with GTP-dependent Rab29, and the two proteins co-localized following stimulation and infection. Rab29 overexpression inhibited NF-κB activation and IL-6 production, while Rab29 deficiency increased both, opposing TBC1D9's effect. Necrotizing soft tissue infection patients' datasets showed upregulation of TBC1D9 and IL-6-related pathways, revealing their clinical relevance. Conclusion: The TBC1D9-Rab29 axis connects GTPase signaling and membrane trafficking to specifically regulate IL-6 in epithelial cells, revealing a non-traditional mechanism for modulating inflammation and a potential target in IL-6-driven diseases.
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