Rheumatism (RA) is a common self-immunological disease with complex and not yet fully defined mechanisms. This paper will explore in depth the mechanisms for the development of rheumatism arthritis from genetic, environmental, self-immunization and cytological factors.
Genetic factors play an important role in the incidence of rheumatism. Studies have shown a significant family concentration of rheumatism, and the risk of disease among first-degree relatives has increased significantly. This suggests that specific genetic variations may make individuals more sensitive to rheumatism. For example, HLA-DR4 genes are closely related to the susceptibility of rheumatism arthritis, and those carrying these genes may be more vulnerable to the effects of environmental factors.
Environmental factors are also considered to be one of the major factors in the incidence of rheumatism. Infections, especially of certain bacteria, viruses and secondary bodies, may trigger the onset of rheumatism. These pathogens may induce the organism to develop an immune response to its own organization through molecular simulation mechanisms. In addition, smoking has been identified as an important environmental risk factor for rheumatism, which not only induces lung damage, but may also contribute to the production of antibodies, thus exacerbating the condition.
Self-immunization responses are at the heart of the rheumatism arthritis system. The patient ‘ s immune system wrongly treated its normal joints as external antigens for attacks, resulting in inflammation of the joints ‘ cartilages, filaments, etc. This anomalous immune response may involve the interaction of multiple immune cells and immune molecules. For example, T- and B-cells are abnormally activated in the joints, producing a large number of their own antibodies, such as the rheumatizer (RF) and the anti-CP antibodies, which misidentify and attack the joints and cause inflammation.
Cell factors also play a key role in the onset of rheumatism. The inflammatory response attracts a large number of inflammatory cells, such as T-cells, megacormic cells and tree tattery cells, which gather at joints and release a variety of cell factors, such as IL-1, IL-6 and TNF-α. These factors not only exacerbate the inflammation process, but may also lead to the destruction of the joint cartilage and bone tissue, which eventually leads to joint deformation and rigidity.
In general, the system for the onset of rheumatism involves genetic, environmental, self-immunization and cytological factors. These factors interact and together lead to disease and development. Although there is currently no complete cure for rheumatism, we can provide a theoretical basis for developing a more effective treatment strategy by in-depth knowledge of its mechanisms. At the same time, care should be taken to avoid inducing factors such as cessation of smoking and maintenance of good living habits in order to reduce the risk of disease and improve the quality of life.
