Failure of Immune System in Rheumatoid Arthritis

Millions of people around the world suffer from rheumatoid arthritis, but the only thing doctors can do is to help patients to cope with the symptoms. The tasks of the scientific and medical community is to stop or to slow down the destruction of the joints of people who have this disease and to make the patients’ lives as comfortable as possible. But it requires deep understanding of the biology of the disease that restricts the movement of patients.

Arthritis is a general term for several inflammatory joint diseases. And because of that there are many reasons for the development of it. A disease called rheumatoid arthritis is caused by joint damage by immune cells that attack the body’s own tissues. It causes the development of edema and overgrowth of the joint tissues that later lead to its deformation. Unfortunately, there has not been invented any “magic pill” that can cure the disease. Modern medical practice assumes just treatment of symptoms that allows stopping pain and suppressing inflammatory reaction. In addition, doctors have to deal with numerous complications accompanying this disease, for example, kidney failure and infections. The factors leading to the development of rheumatoid arthritis are still not fully known. Nevertheless, it is clear that people who have this disease also have genetic and epigenetic predisposition to it. Moreover, the trigger factor for the development of rheumatoid arthritis is stress.

Immune system provokes the development of the disease

Doctors have not found out yet why the joints begin to get inflamed. It is only known that some kind of push to the onset of the disease gives rise to a malfunction in the immune system. Usually immune system uses antibodies to protect the body against diseases and infections, but in the case of rheumatoid arthritis the antibodies that have been produced with no evident reason “erroneously” attack the joints. Usually rheumatoid arthritis affects the joints of hands. The cells of the immune system migrate into the joint bag, causing its inflammation, or synovitis. Inflammation leads to destruction of cartilage and further erosion of bone tissue. As cartilaginous tissue is practically incapable of regeneration, and bone tissue is greatly deforming during permanent processes of destruction and regeneration, rheumatoid lesions remain with the patients for life. So, what can cause such abnormal behavior of immune system?

Genetics has an answer

Predisposition to rheumatoid arthritis is greatly affected by the genes of the major histocompatibility complex. Proteins encoded by these genes are responsible for presenting the antigen to T-lymphocytes. Some of their variants can carry out this process more effectively with respect to their own antigens, thus, promoting the start of the autoimmune process. HLA-DRB1 gene is one of the most interesting genes of this group. It encodes the components of HLA-DR surface receptor interacting with the T-cell receptor. Also, the interaction of specific variants of different genes (for example, HLA-DRB1 and PTPN22) increases the likelihood of the disease. Epigenetic mechanisms can also regulate the functioning of the immune system increasing the risk of development of rheumatoid arthritis. These mechanisms lead to a change in the usual work of key genes involved in pathogenesis.

Rheumatoid arthritis is a disease that has not been completely studied yet and because of that it cannot be treated now. Scientists need some more time to understand the nature and causes of this disease to introduce any effective treatment.