ORCID Profile
0000-0002-7301-9699
Current Organisations
Centre Hospitalier Universitaire de Besançon
,
Karolinska Institutet
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Publisher: Wiley
Date: 19-09-2020
DOI: 10.1111/SJI.12953
Abstract: Psoriasis is an inflammatory disease that arises in genetically predisposed in iduals. Chronic skin lesions that contain activated immune cells can persist for years. Systemic inhibition of TNF, IL‐17 and IL‐23 cytokines has revolutionized psoriasis care during the recent decades. Unfortunately, local relapse of disease is common at previously inflamed sites after cessation of treatment. This highlights that fundamental pathologic alterations of the affected tissues are not completely resolved during clinical remission. Here, we present arguments for a local disease memory located in both dermis and epidermis in psoriasis skin. We decipher different cellular components and intercellular crosstalk that sustain local disease memory and lify disease relapse in human psoriasis. Decrypting the mechanisms underlying the establishment and persistence of pathogenic memory cells in resolved psoriasis may provide new therapeutic perspectives aimed at long‐term remission of psoriasis.
Publisher: Elsevier BV
Date: 02-2017
Publisher: Wiley
Date: 23-03-2017
DOI: 10.1111/EXD.13225
Publisher: Elsevier BV
Date: 04-2017
DOI: 10.1016/J.JID.2016.11.033
Abstract: Epidermal Langerhans cells (LCs) are spatially separated from dermal dendritic cells (DCs) in healthy human skin. In active psoriasis, maintained by local production of IL-23 and IL-17, inflammatory DCs infiltrate both skin compartments. Here we show that CCR2
Publisher: Elsevier BV
Date: 08-2018
DOI: 10.1016/J.JID.2018.02.030
Abstract: Psoriasis is driven by focal disruptions of the immune-homeostasis in human skin. Local relapse following cessation of therapy is common and unpredictable, which complicates clinical management of psoriasis. We have previously shown that pathogenic resident T cells accumulate in active and resolved psoriasis, but whether these cells drive psoriasiform tissue reactions is less clear. Here, we activated T cells within skin explants using the pan-T cell activating antibody OKT-3. To explore if T cells induced different tissue response patterns in healthy and psoriasis afflicted skin, transcriptomic analyses were performed with RNA-sequencing and Nanostring. Core tissue responses dominated by IFN-induced pathways were triggered regardless of the inflammatory status of the skin. In contrast, pathways induced by IL-17A, including Defensin beta 2 and keratinocyte differentiation markers, were activated in psoriasis s les. An integrated analysis of IL-17A and IFN-related responses revealed that IL-17 dominated tissue response correlated with early relapse following UVB treatment. Stratification of tissue responses to T cell activation in resolved lesions could potentially offer in idualized prediction of disease relapse during long-term immunomodulatory treatment.
Publisher: Wiley
Date: 09-2022
DOI: 10.1111/ALL.15484
No related grants have been discovered for Irène Gallais Sérézal.