Immune-mediated experimental arthritis in IL-33 deficient mice.
Cytokine
; 69(1): 68-74, 2014 Sep.
Article
en En
| MEDLINE
| ID: mdl-25022964
ABSTRACT
Previous work suggested implication of the interleukin (IL)-1 family cytokine IL-33, signaling through its receptor ST2, in the pathogenesis of human and mouse arthritis. In this study, we directly investigated the role of endogenous IL-33 in antigen-induced arthritis (AIA) and collagen-induced arthritis (CIA) using IL-33 KO mice. AIA was induced by injection of methylated bovine serum albumin (mBSA) into knee joints of previously immunized mice. CIA was induced by immunization with bovine type II collagen. Disease severity was evaluated by clinical and histological scoring and cellular immune responses were assessed in cultured draining lymph node cells. Our results indicate that the development of AIA or CIA, as assessed by clinical or histological evaluation, is not impaired in IL-33 deficient mice. We did not observe any consistent modifications in humoral or cellular immune responses in IL-33 KO mice, although IL-33 deficiency enhanced antigen-specific IFN-γ production, proliferation or IgG2a titers in some experiments, suggesting that endogenous IL-33 may contribute to shaping the adaptive immune response. In conclusion, our data suggest that IL-33 plays a modifying rather than a pivotal role in disease development in two models of immune-mediated arthritis.
Palabras clave
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Artritis Experimental
/
Interleucinas
/
Inmunidad Adaptativa
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Cytokine
Asunto de la revista:
ALERGIA E IMUNOLOGIA
Año:
2014
Tipo del documento:
Article
País de afiliación:
Suiza