protease activity is required for FcγR-induced arthritis but not FcγR-mediated platelet elimination in mice.

Fc receptors for IgGs (FcγRs) play important roles both in protective and pathogenic immune responses. The assembly of the CARD9/BCL10/MALT1 signalosome is required for optimal FcγR-induced canonical NF-κB activation and pro-inflammatory cytokine release.

Our goal was to clarify the relevance of the MALT1 protease activity in FcγR-driven events and the therapeutic potential of selective MALT1 protease inhibitors in FcγR-mediated diseases.Using genetic and pharmacological disruption of MALT1 scaffolding and enzymatic activity, we assessed the relevance of MALT1 function in murine and human primary myeloid cells upon stimulation with immune complexes (IC) and using murine models of autoantibody-driven arthritis and immune thrombocytopenic purpura (ITP).

[Linking template=”default” type=”products” search=”ICT-651″ header=”2″ limit=”120″ start=”2″ showCatalogNumber=”true” showSize=”true” showSupplier=”true” showPrice=”true” showDescription=”true” showAdditionalInformation=”true” showImage=”true” showSchemaMarkup=”true” imageWidth=”” imageHeight=””]