Rheumatism arthritis (RA), a common and complex self-immunological disease, has long plagued a large number of patients, and in recent years there have been many noteworthy research advances in its morbidity mechanisms and clinical treatment.
At the institutional level, the exceptional activation of the immune system is at the core. First, genetic factors have been shown to have important effects, and the associated genes of human white cell antigens (HLA), such as HLA-DR4, can make individuals susceptible to rheumatism. People carrying these genes are more vulnerable to immunosuppressive imbalances when their immune systems are stimulated from the outside. Infective factors in environmental factors, such as the EB virus, bacteria and other pathogens that are infected with the human body, may lead to an “misidentification” of the immune system in the fight against infection, misusing the arthromic tissue and so forth as a foreign harmful substance, which can cause inflammation.
In addition, cytological network disorders play a key role in morbidity mechanisms. Inflammatory factors such as tumour necrosis – alpha (TNF-α), white cell medium – 1 (IL-1) and white cell medium – 6 (IL-6) are produced in large numbers. They constantly stimulate the growth and activation of the slide membranes into fibre cells, which contribute to the increase of their degenerative substrate metallic protein enzymes, etc., and damage joint cartilage and bone tissues. At the same time, immuno-modified cell abnormalities such as modulated T-cells are not effective in inhibiting excessive immune reactions, which perpetuates and continues to develop inflammable lesions leading to irreversible lesions at the joints.
Progress has also been significant in clinical treatment. Traditional rheumatoids (DMARDs) continue to be the basis of treatment, such as aminotrile, which controls the development of the disease by inhibiting cell proliferation and regulating the immune response, although they work relatively slowly and may be accompanied by some adverse effects in long-term use.
The emergence of biological agents has been a major breakthrough in recent years. For example, single-cloned antibodies for TNF-α, such as the Influenza Monovalence, the Adawood Monovalence, etc., can accurately disrupt the activity of TNF-α, rapidly and effectively reduce arthritis, relieve pain and improve joint function, and significantly improve the quality of life of patients. Biological agents targeting other cytogens or immunocellular surface molecules are also being developed and used to provide more options for patients with different conditions.
Small molecular targeting drugs are also emerging therapeutic forces, such as JAK inhibitors, which, by inhibiting the activity of Janus radical enzymes, block the transmission of relevant signals within cells, influence the function of immunocells and the generation of cytofactors, ease of use, oral administration of drugs, and demonstrate good efficacy in improving the condition.
However, despite the many advances in understanding and treatment of the rheumatological arthritis outbreak mechanisms, challenges remain, such as how to further reduce the side effects of drugs and achieve individualized precision treatment. The future needs to be constantly and in-depth, working tirelessly to fight the disease.
