IL-12 inhibits endotoxin-induced inflammation in the eye

IL-12 inhibits endotoxin-induced inflammation in the eye

Autor Whitcup, S. M. Google Scholar
Rizzo, L. V. Google Scholar
Lai, J. C. Google Scholar
Hayashi, S. Google Scholar
Gazzinelli, R. Google Scholar
Chan, C. C. Google Scholar
Instituição NIH
Universidade Federal de São Paulo (UNIFESP)
NIAID
Universidade Federal de Minas Gerais (UFMG)
Resumo Interleukin-12 (IL-12) is a heterodimeric cytokine that induces interferon (IFN)-gamma production and an increased generation of Th 1 cells. Both IL-12 and IL-12 antagonists are being studied for the treatment of allergic reactions, autoimmune disease and malignancy. the goal of the present experiments was to examine the importance of IL-12 in endotoxin-induced ocular inflammation. the number of inflammatory cells infiltrating eyes with endotoxin-induced uveitis (EIU) was significantly increased in animals treated with intraperitoneal anti-IL-12 antibody when compared to control animals, but there was no difference in infiltrating inflammatory cells in the eyes of animals treated with IL-12 when compared to controls. in contrast, intraocular injection of IL-12 significantly inhibited the development of endotoxin-induced intraocular inflammation. the inflammatory cells were reduced in the eves of animals receiving intraocular IL-obtained from eyes with EIU showed increased levels of IFN-gamma and decreased levels of IL-6 in eyes receiving intraocular IL-12. These data show that IL-12 has an inhibitory effect on endotoxin-induced inflammation in the eye and su that IL-12 can have an immunoregulatory function in some forms of inflammatory disease.
Palavra-chave interleukin-12
endotoxin
eye
inflammation
cytokine
Idioma Inglês
Data de publicação 1996-05-01
Publicado em European Journal of Immunology. Deerfield Beach: Vch Publishers Inc, v. 26, n. 5, p. 995-999, 1996.
ISSN 0014-2980 (Sherpa/Romeo, fator de impacto)
Publicador Vch Publishers Inc
Extensão 995-999
Fonte http://dx.doi.org/10.1002/eji.1830260506
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:A1996UT53100005
Endereço permanente http://repositorio.unifesp.br/handle/11600/25582

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