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Pro and anti-cytokine in Psoriasis

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HAL Id: hal-02739839

https://hal.inrae.fr/hal-02739839

Submitted on 2 Jun 2020

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Pro and anti-cytokine in Psoriasis

Gregory Bouchaud

To cite this version:

Gregory Bouchaud. Pro and anti-cytokine in Psoriasis. Allergolyon, Université Claude Bernard Lyon 1 (UCBL). Lyon, FRA. Institut National de la Santé et de la Recherche Médicale (INSERM). Centre Hospitalier Lyon Sud [CHU - HCL], FRA., Jan 2015, Lyon, France. �hal-02739839�

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Psoriasis is a chronic, inflammatory skin disease affecting 2 to 3% of the white population. It is a multifactorial disease since its development depends on a complex interplay of genetic and environmental factors. As no pathogen has been consistently identified within psoriatic plaques, an autoimmune basis for the chronic inflammation is the dogma for this complex disorder. Psoriasis is characterized by macroscopic and microscopic skin alterations and leads to considerable impairment of the quality of life of the affected patients. Cutaneous and systemic over-expression of various pro-inflammatory cytokines has been demonstrated in psoriasis. For instance, psoriatic keratinocytes are able to produce and release IL-1, IL-6, IL-15, IL-18 and IL- 20, all of them involved in the development of different alterations which compose the complex and intricate net of psoriasis pathogenesis. T cells also mediate the psoriasis pathogenesis by secreting an array of cytokines, including tumor necrosis factor-α (TNF), interferon-γ (IFN-γ), IL-17, and IL-22, to stimulate proliferation of keratinocytes and recruit inflammatory cells. The cellular composition of the inflammatory infiltrate within the psoriatic plaques as well as hyperproliferation of keratinocytes and so the whole pathogenetic process of psoriasis appears to be mediated by cytokines. The source and the mechanisms of action of pro and anti- inflammatory cytokine underlying psoriasis in humans and in mouse models are poorly understood. In this context, the role of different cytokine will be presented with a special focus on the new IL17/IL-23 axis and the unexpected role of IL-15 in mouse models of skin inflammation and in human.

Bibliography

-Bouchaud G, Gehrke S, Krieg C, Kolios A, Hafner J, Navarini AA, French LE, Boyman O: Epidermal IL-15Ralpha acts as an endogenous antagonist of psoriasiform inflammation in mouse and man. J Exp Med 2013, 210:2105-2117.

-Ha HL, Wang H, Pisitkun P, Kim JC, Tassi I, Tang W, Morasso MI, Udey MC, Siebenlist U: IL-17 drives psoriatic inflammation via distinct, target cell-specific mechanisms. Proc Natl Acad Sci U S A 2014, 111:E3422-3431.

-Lowes MA, Suarez-Farinas M, Krueger JG: Immunology of psoriasis. Annu Rev Immunol 2014, 32:227-255.

-Ueyama A, Yamamoto M, Tsujii K, Furue Y, Imura C, Shichijo M, Yasui K:

Mechanism of pathogenesis of imiquimod-induced skin inflammation in the mouse: a role for interferon-alpha in dendritic cell activation by imiquimod. J Dermatol 2014, 41:135-143.

-Yoshiki R, Kabashima K, Honda T, Nakamizo S, Sawada Y, Sugita K, Yoshioka H,

Ohmori S, Malissen B, Tokura Y, Nakamura M: IL-23 from Langerhans cells is

required for the development of imiquimod-induced psoriasis-like dermatitis by

induction of IL-17A-producing gammadelta T cells. J Invest Dermatol 2014,

134:1912-1921.

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