Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 138, Issue 8, Pages 1754-1763Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2018.02.030
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Funding
- Swedish Research Council
- Ragnar Soderberg Stiftelse
- Svenska Lakarsallskapet
- Stockholm County Council (ALF)
- Psoriasisfonden
- Hudfonden
- Marcus and Marianne Wallenberg Foundation
- Karolinska Institutet (KID)
- Societe Francaise de Dermatologie
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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 samples. 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 individualized prediction of disease relapse during long-term immunomodulatory treatment.
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