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Immune-mediated experimental arthritis in IL-33 deficient mice.

Cytokine (2014-07-16)
Dominique Talabot-Ayer, Praxedis Martin, Christian Alexander Seemayer, Solenne Vigne, Céline Lamacchia, Axel Finckh, Essia Saiji, Cem Gabay, Gaby Palmer
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.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Mouse IL-10 ELISA Kit, for serum, plasma and cell culture supernatant
Sigma-Aldrich
Human IL-10 ELISA Kit
Sigma-Aldrich
Human IL-10 R β ELISA Kit, for serum, plasma, cell culture supernatant and urine
Sigma-Aldrich
Rat IL-10 ELISA Kit, for cell and tissue lysates
Sigma-Aldrich
Rat IL-10 ELISA Kit, for serum, plasma and cell culture supernatant