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Suppression of innate inflammation and immunity by interleukin-37.
Dinarello, Charles A; Nold-Petry, Claudia; Nold, Marcel; Fujita, Mayumi; Li, Suzhao; Kim, Soohyun; Bufler, Philip.
Afiliação
  • Dinarello CA; University of Colorado Denver, Aurora, CO, USA.
  • Nold-Petry C; Radboud University Medical Center, Nijmegen, The Netherlands.
  • Nold M; Monash University, Melbourne, Australia.
  • Fujita M; Monash University, Melbourne, Australia.
  • Li S; University of Colorado Denver, Aurora, CO, USA.
  • Kim S; University of Colorado Denver, Aurora, CO, USA.
  • Bufler P; University of Colorado Denver, Aurora, CO, USA.
Eur J Immunol ; 46(5): 1067-81, 2016 05.
Article em En | MEDLINE | ID: mdl-27060871
IL-37 is unique in the IL-1 family in that unlike other members of the family, IL-37 broadly suppresses innate immunity. IL-37 can be elevated in humans with inflammatory and autoimmune diseases where it likely functions to limit inflammation. Transgenic mice expressing human IL-37 (IL37-tg) exhibit less severe inflammation in models of endotoxin shock, colitis, myocardial infarction, lung, and spinal cord injury. IL37-tg mice have reduced antigen-specific responses and dendritic cells (DCs) from these mice exhibit characteristics of tolerogenic DCs. Compared to aging wild-type (WT) mice, aging IL37-tg mice are protected against B-cell leukemogenesis and heart failure. Treatment of WT mice with recombinant human IL-37 has been shown to be protective in several models of inflammation and injury. IL-37 binds to the IL-18 receptor but then recruits the orphan IL-1R8 (formerly TIR8 or SIGIRR) in order to function as an inhibitor. Here, we review the discovery of IL-37, its production, release, and mechanisms by which IL-37 reduces inflammation and suppresses immune responses. The data reviewed here suggest a therapeutic potential for IL-37.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interleucina-1 / Imunidade Inata / Inflamação Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Eur J Immunol Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Interleucina-1 / Imunidade Inata / Inflamação Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Eur J Immunol Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Estados Unidos