A study published online this week in the journal Science Translational Medicine, lends new credence to the hypothesis that immune pathways activated in response to pathogens play a role in initiating immune responses in rheumatoid arthritis. Researchers found that two pore-forming pathways in cell membranes, known as perforin and membrane attack complex (MAC), are active contributors in generating the targets to the immune response, or auto-antigens, thought to initiate and maintain inflammation in rheumatoid arthritis. Inhibiting these pathways may open up new avenues for treatment of the autoimmune condition. Read more about the study here.
Posted on November 1, 2013