Type II collagen is abundant in the joint and is a major target of immune-mediated damage in RA. As suggested in studies of experimental animals, induction of immune tolerance at the level of the cartilage may be a way of reducing the signs and symptoms of RA and prevent joint destruction. However, whether oral administration of Type II collagen is an efficacious treatment for humans with established active RA has not been established.
Bone erosions in response to inflammation in RA are driven by osteoclasts which are in turn activated by RANKL (Receptor Activator for Nuclear Factor κ B Ligand) binding to its receptor RANK. Inhibition of RANKL has the potential to retard bone erosions in RA patients, thereby limiting progressive joint damage and destruction.
Estrogens are known to modify immunologic responses and the modulation of rheumatoid arthritis (RA) disease activity during pregnancy is well documented. However, whether physiologic replacement of estrogen and other hormones after menopause adversely affects RA outcomes is controversial.
Susceptibility to rheumatoid arthritis (RA) is complex; although a number of genetic susceptibility loci have been identified that appear to confer increased risk. Among these, genes encoding sequence variants in the major histocompatibility complex (MHC) class II molecule, known as the “shared epitope” (SE), have been known for decades and have the strongest link to RA susceptibility.
Atacicept is a recombinant fusion protein that binds and neutralizes two molecules important for the maturation, proliferation, and survival of B cells: BLyS and APRIL. While B-cell depleting therapies have demonstrated efficacy in RA, atacicept differs from the anti-CD20 targeted monoclonal antibodies, such as rituximab, as its effects extend over the entire lineage of B lymphocytes, including plasma cells.