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Increased circulating pro-inflammatory cytokines and imbalanced regulatory T-cell cytokines production in chronic idiopathic urticaria

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Autor(es):
dos Santos, Juliana Cristina ; Azor, Mayce Helena ; Nojima, Viviane Yoshimi ; Lourenco, Francinelson Duarte ; Prearo, Erica ; Maruta, Celina Wakisaka ; Rivitti, Evandro Ararigboia ; da Silva Duarte, Alberto Jose ; Sato, Maria Notomi
Número total de Autores: 9
Tipo de documento: Artigo Científico
Fonte: International Immunopharmacology; v. 8, n. 10, p. 8-pg., 2008-10-01.
Resumo

The immunologic characterization of chronic idiopathic urticaria (CIU), mainly regarding cytokine profile needs more investigation. We examined circulating inflammatory cytokine levels, T-cell induced secretion, and cytokine mRNA expression in patients with CIU subjected to the intradermal autologous serum skin test (ASST). Increased levels of circulating pro-inflammatory cytokines, such as TNF-alpha, IL-1 beta, IL-12p70, and IL-6 have been observed in most of patients with CIU, together with an enhancement of IL-2 secretion following T-cell stimulation. Highlighting the inflammatory profile in CIU found in ASST positive, is the enhanced B-cell proliferative responsiveness and increased IL-17 secretion levels. ASST-positive patients also exhibited impaired IL-4 secretion associated with increased IL-10 production. Altered cytokine expression in patients with ASST-negative, was the down-modulation of spontaneous IL-10 mRNA expression levels in peripheral blood mononuclear cells. Our findings support the concept of immunologic dysregulation in CIU, revealing a systemic inflammatory profile associated with disturbed cytokine production by T cells, mainly related to IL-17 and IL-10 production. (c) 2008 Elsevier B.V. All rights reserved. (AU)

Processo FAPESP: 04/06937-5 - Evidência de auto-anticorpos anti-receptores de alta afinidade para IgE na urticária crônica: análise da expressão do receptor em basófilos, produção de citocinas e o potencial imunomodulatório de oligonucleotídeos CpG
Beneficiário:Maria Notomi Sato
Modalidade de apoio: Auxílio à Pesquisa - Regular