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.

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.
References:
Rheumatoid arthritis – MAYO Clinic
Arthritis Foundation – materials
How your immune system works : The basics – RA
Rheumatoid Arthritis When Your Immune System Attacks Your Body – NIH Medline Plus
Epigenetics in the pathogenesis of rheumatoid arthritis – NCBI