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Gaby Palmer

Researcher at University of Geneva

Publications -  111
Citations -  7591

Gaby Palmer is an academic researcher from University of Geneva. The author has contributed to research in topics: Inflammation & Arthritis. The author has an hindex of 43, co-authored 99 publications receiving 6767 citations. Previous affiliations of Gaby Palmer include Geneva College.

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IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells

TL;DR: These findings point toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo.
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The IL-1 receptor accessory protein (AcP) is required for IL-33 signaling and soluble AcP enhances the ability of soluble ST2 to inhibit IL-33.

TL;DR: Immunoprecipitation confirmed that IL-33 specifically binds ST2 and revealed that cellular IL-1 receptor accessory protein (AcP) associates with ST2 in a ligand-dependent manner, identifying AcP as a shared co-receptor within theIL-1 family that is essential for IL-32 signaling and suggesting a novel role for sAcP in modulating the activity of IL- 33.
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Evidence for a role of p38 MAP kinase in expression of alkaline phosphatase during osteoblastic cell differentiation

TL;DR: The data indicate that MAPKs regulate different stages of MC3T3-E1 cell development in response to FCS, with Erk playing an essential role in cell replication, whereas p38 is involved in the regulation of ALP expression during osteoblastic cell differentiation.
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Is IL-1 a good therapeutic target in the treatment of arthritis?

TL;DR: IL-1 blockade by anakinra is dramatically effective in systemic-onset juvenile idiopathic arthritis, in adult Still's disease and in several autoinflammatory disorders, most of the latter being caused by mutations of proteins controlling IL-1beta secretion.
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The new IL-1 family member IL-1F8 stimulates production of inflammatory mediators by synovial fibroblasts and articular chondrocytes.

TL;DR: IL-1F8 exerts proinflammatory effects in primary human joint cells, and it remains to be determined whether circulating IL-1f8 can contribute to joint inflammation in rheumatoid arthritis.