Cytokine-Mediated Crosstalk Between Keratinocytes and T Cells in Atopic Dermatitis - PubMed (original) (raw)

Review

Cytokine-Mediated Crosstalk Between Keratinocytes and T Cells in Atopic Dermatitis

Mélanie Humeau et al. Front Immunol. 2022.

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by barrier dysfunction, dysregulated immune response, and dysbiosis with increased Staphylococcus aureus colonization. Infiltration of various T helper cell subsets into lesional skin and subsequent cytokine release are a hallmark of AD. Release of cytokines by both T cells and keratinocytes plays a key role in skin inflammation and drives many AD features. This review aims to discuss cytokine-mediated crosstalk between T cells and keratinocytes in AD pathogenesis and the potential impact of virulence factors produced by Staphylococcus aureus on these interactions.

Keywords: T cells; atopic dermatitis (AD); cytokines; keratinocytes; staphylococcus aureus.

Copyright © 2022 Humeau, Boniface and Bodet.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1

Figure 1

Impact of cytokine-mediated crosstalk between keratinocytes and T cells on atopic dermatitis features. (A) Involvement of the cytokine-mediated crosstalk in barrier dysfunction and pruritus. Th2, Th17, and Th22 cytokines inhibit differentiation markers and favor itch, leading to barrier disruption, which in return induces secretion of pro-inflammatory cytokine including TSLP, IL-33, and IL-25 by keratinocytes. (B) Involvement of the cytokine-mediated crosstalk in chemoattraction of T cells. The keratinocyte-derived inflammatory mediators include chemokines that lead to chemoattraction of T cells. Attraction of T cells and Th2 response promote a pro-inflammatory cytokine production loop in keratinocytes. (C) Impact of S. aureus on keratinocytes and T cells in atopic dermatitis. Virulence factors produced by S. aureus can promote degradation of junctional adhesion molecules and alteration of keratinocyte differentiation that contribute to atopic skin barrier disruption. S. aureus can also favor a pro-inflammatory environment through Th2 cell infiltration into the skin, pro-inflammatory cytokine release by keratinocytes and T cells as well as by inhibiting Treg immunosuppressive activity. FBP1, fibronectin-binding protein-1; LTA, lipoteichoic acid; PSMs, phenol soluble modulins; SEs, staphylococcal enterotoxins; SspA, serine protease A; TSST-1, toxic shock syndrome toxin-1.

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References

    1. Peters N, Peters AT. Atopic Dermatitis. Allergy Asthma Proc (2019) 40:433–6. doi: 10.2500/aap.2019.40.4265 - DOI - PubMed
    1. Chiesa Fuxench ZC, Block JK, Boguniewicz M, Boyle J, Fonacier L, Gelfand JM, et al. . Atopic Dermatitis in America Study: A Cross-Sectional Study Examining the Prevalence and Disease Burden of Atopic Dermatitis in the US Adult Population. J Invest Dermatol (2018) 139:583–90. doi: 10.1016/j.jid.2018.08.028 - DOI - PubMed
    1. Yang G, Seok JK, Kang HC, Cho Y-Y, Lee HS, Lee JY. Skin Barrier Abnormalities and Immune Dysfunction in Atopic Dermatitis. Int J Mol Sci (2020) 21:2867. doi: 10.3390/ijms21082867 - DOI - PMC - PubMed
    1. Williams MR, Gallo RL. The Role of the Skin Microbiome in Atopic Dermatitis. Curr Allergy Asthma Rep (2015) 15:65. doi: 10.1007/s11882-015-0567-4 - DOI - PubMed
    1. Eichenfield LF, Tom WL, Chamlin SL, Feldman SR, Hanifin JM, Simpson EL, et al. . Guidelines of Care for the Management of Atopic Dermatitis. J Am Acad Dermatol (2014) 70:338–51. doi: 10.1016/j.jaad.2013.10.010 - DOI - PMC - PubMed

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