Increased IL17A, IFNG, and FOXP3 Transcripts in Moderate-Severe Psoriasis: A Major Influence Exerted by IL17A in Disease Severity

Author:

Oliveira Priscilla Stela Santana de1,Pereira Michelly Cristiny1,Silva de Paula Simão Kalebe1,Lima Emerson Vasconcelos Andrade2,Lima Mariana Modesto de Andrade2,Arruda Rodrigo Gomes de3,Oliveira Wagner Luís Mendes de1ORCID,Duarte Ângela Luzia Branco Pinto2,Pitta Ivan da Rocha1,Rêgo Moacyr Jesus Melo Barreto1ORCID,Galdino da Rocha Pitta Maira1ORCID

Affiliation:

1. Laboratório de Imunomodulação e Novas Abordagens Terapêuticas (LINAT), Núcleo de Pesquisa em Inovação Terapêutica Suely Galdino (NUPIT-SG), Universidade Federal de Pernambuco (UFPE), Recife, PE, Brazil

2. Hospital das Clínicas, Universidade Federal de Pernambuco (UFPE), Recife, PE, Brazil

3. Faculdade Nova Roma, Recife, PE, Brazil

Abstract

Psoriasis is a chronic and recurrent dermatitis, mediated by keratinocytes and T cells. Several proinflammatory cytokines contribute to formation and maintenance of psoriatic plaque. The Th1/Th17 pathways and some of IL-1 family members were involved in psoriasis pathogenesis and could contribute to disease activity. Therefore, we sought to analyse skin transcript levels of IL17A, IL22, RORC, IL8, IFNG, IL33, IL36A, FOXP3, and IL10 and correlate with clinic of patients with plaque-type psoriasis. In order to conduct that, we collected punch biopsies from lesional skin and obtained tissue RNA. After reverse transcription, qRT-PCR quantified the relative mRNA expression. The main results revealed increased transcripts levels of IL17A, IFNG, and FOXP3 in moderate-severe patients. Despite this, only IL17A can increase the chance to worsen disease severity. We also observed many significant positive correlations between each transcript. In conclusion, IL17A is elevated in lesional skin from psoriasis patients and plays crucial role in disease severity.

Funder

Instituto Nacional de Ciência e Tecnologia para Inovação Farmacêutica

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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