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English: Potential role of chronic physical exercise on immune system modulation in vitiligo patients. Physical exercise can induce skeletal muscle to release huge amounts of IL-6, which has the potential to reach the skin and induce a local adaptation of the immune system (anti-inflammatory profile). For example, hypothetically high amounts of IL-6 in the skin can be detected by skin-resident APC and regulatory T cells that, in turn, give negative feedback releasing IL-10. IL-10 can inhibit the local production of IL-1, IFN-γ, and TNF-α. Inhibiting IL-1-β and TNF-α, there is no negative feedback for CTLA-4 expression in cytotoxic T cells (the interaction between CTL-4 from CD8+ T cell with costimulatory molecule B7 from APC suppress CD8+ T cell activation). Also, IL-10 could inhibit CD8+ T cells by inhibiting the expression of costimulatory class II MHC molecules from APC. IL-6 also induces significant TGF-β expression, resulting in upregulation of FoxP3. APC, antigen-presenting cell; CD28, Cluster of Differentiation 28; CTLA-4, cytotoxic T lymphocyte antigen-4; CXCL, C-X-C motif chemokine ligand; CXCR, C-X-C motif chemokine receptor; DAMPs, damage-associated molecular pattern; JAK/STAT, Janus kinase/signal transducer and activator of transcription; IFN-γ, interferon-gamma; IL, interleukin; MHC, major histocompatibility complex; TGF-β, transforming growth factor, TNF-α, tumor necrosis factor-alpha.
Español: Papel potencial del ejercicio físico crónico en la modulación del sistema inmunológico en pacientes con vitíligo. El ejercicio físico puede inducir al músculo esquelético a liberar enormes cantidades de IL-6, que tiene el potencial de llegar a la piel e inducir una adaptación local del sistema inmunológico (perfil antiinflamatorio). Por ejemplo, las APC residentes en la piel y las células T reguladoras pueden detectar cantidades hipotéticamente altas de IL-6 en la piel que, a su vez, dan retroalimentación negativa al liberar IL-10. La IL-10 puede inhibir la producción local de IL-1, IFN-γ y TNF-α. Al inhibir IL-1-β y TNF-α, no hay retroalimentación negativa para la expresión de CTLA-4 en células T citotóxicas (la interacción entre CTL-4 de células T CD8+ con la molécula coestimuladora B7 de APC suprime la activación de las células T CD8+). Además, la IL-10 podría inhibir las células T CD8+ al inhibir la expresión de moléculas MHC coestimuladoras de clase II de APC. IL-6 también induce una expresión significativa de TGF-β, lo que resulta en una regulación positiva de FoxP3. APC, célula presentadora de antígeno; CD28, grupo de diferenciación 28; CTLA-4, antígeno 4 de linfocitos T citotóxicos; CXCL, ligando de quimiocina con motivo C-X-C; CXCR, receptor de quimiocina con motivo C-X-C; DAMP, patrón molecular asociado a daños; JAK/STAT, Janus quinasa/transductor de señal y activador de la transcripción; IFN-γ, interferón-gamma; IL, interleucina; MHC, complejo mayor de histocompatibilidad; TGF-β, factor de crecimiento transformante, TNF-α, factor de necrosis tumoral alfa.
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Source https://www.frontiersin.org/articles/10.3389/fphys.2022.843784/full
Author Frontiers

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current23:58, 5 December 2023Thumbnail for version as of 23:58, 5 December 20234,317 × 2,499 (544 KB)AbchyZa22 (talk | contribs)Uploaded a work by Frontiers from https://www.frontiersin.org/articles/10.3389/fphys.2022.843784/full with UploadWizard