cIAP1/2 inhibition synergizes with TNF inhibition in autoimmunity by down-regulating IL-17A and inducing T.

IL-17 and TNF-α are major effector cytokines in chronic inflammation. TNF-α inhibitors have revolutionized the treatment of rheumatoid arthritis (RA), although not all patients respond, and most relapse after treatment withdrawal. This may be due to a paradoxical exacerbation of T17 responses by TNF-α inhibition.

T cell activation Rho GTPase activating protein (TAGAP) is upregulated in clinical and experimental arthritis.

Genome-wide association studies have identified various susceptibility variants and loci associated with incidence of rheumatoid arthritis (RA) in different populations. One of these is T cell activation Rho GTPase activating protein (TAGAP). The present study sought to measure the expression of TAGAP in RA patients, CD4 T cells subsets from healthy humans and in mice with collagen-induced arthritis.

Targeted IL-4 therapy synergizes with dexamethasone to induce a state of tolerance by promoting Treg cells and macrophages in mice with arthritis.

F8-IL-4 is a recently developed immunocytokine that delivers IL-4 to sites of inflammation by targeting the neovasculature. We previously reported that F8-IL-4, in combination with dexamethasone (DXM), provides a durable therapy in mice with collagen-induced arthritis (CIA). Therefore, the objective of this study was to identify the mechanism by which IL-4 and DXM combination therapy provides long-lasting disease remission.