GPR91 deletion enhances mast cell activation while preventing arthritic disease

While searching for a role of succinate on skin inflammation we discovered that its specific receptor, GPR91/SUCNR1 is also expressed by mast cells. Sucnr1-/- mast cells displayed enhanced reactivity to allergen-IgE crosslinking. However, such responses were acute in nature and did not contribute to the enhancement of asthma or arthritis and, we therefore suggest, they are due to alterations during mast cell differentiation. The fact that sucnr1-/- mice were protected from arthritis development, using two different in vivo models, indicates that GPR91 antagonists may have great therapeutic potential in autoimmune disease