Systemic lupus erythematosus (SLE) is a complex autoimmune disease, and its morbidity mechanism is not yet fully understood, but it is considered to be the result of the interaction of genetic, environmental, infectious, sex hormone and immune system abnormalities.
First, genetic factors play an important role in the morbidity of systemic lupus erythematosus. Studies have shown that people with family history have a significantly increased risk of systemic lupus erythematosus. Certain genes, such as HLA-DR2 and HLA-DR3, are associated with susceptibility to disease. Although genetic factors are not the only determinants, they provide an internal basis for the occurrence of diseases. For example, in some families, there may be mutations or abnormal expression of certain genes, which make family members more vulnerable to external factors and morbidity.
Environmental factors are also one of the important factors inducing systemic lupus erythematosus. UV exposure is the most common environmental trigger. Ultraviolet light can damage skin cells and expose nuclear antigens in cells, thus triggering abnormal immune system responses. Some drugs such as hydralazine and penicillamine may also cause systemic lupus erythematosus. In addition, chemical reagents and biological products are also related to the occurrence of diseases. Long-term exposure to these substances may alter the body’s immune status, prompting the immune system to attack its own tissues.
Infection factors can not be ignored in the morbidity of systemic lupus erythematosus. Infection with certain pathogens, such as streptococcus and Epstein-Barr virus, may lead to disorders of the immune system. When these pathogens enter the body, the immune system produces an immune response to fight them. However, in some cases, this immune response may be overactivated or deregulated, triggering an immune attack on one’s own tissues. For example, immune complexes may be deposited in tissues after infection, causing an inflammatory response and tissue damage.
Sex hormone levels are closely related to the morbidity of systemic lupus erythematosus. The incidence of female patients is significantly higher than that of male patients, especially in women of childbearing age. This may be because women have higher levels of estrogen, which can affect the function of the immune system. Estrogen may promote the activation of B cells and the production of autoantibodies, thus increasing the risk of disease.
Immune dysfunction is the core mechanism of morbidity in systemic lupus erythematosus. Under normal circumstances, the immune system can accurately recognize foreign pathogens and attack them, while maintaining immune tolerance to its own tissues. However, in patients with systemic lupus erythematosus, the immune system is abnormal. B cells are over-activated and produce a large number of autoantibodies against their own tissues, such as antinuclear antibodies, anti-double-stranded DNA antibodies and so on. These autoantibodies combine with autoantigens to form immune complexes, which deposit in the skin, joints, kidneys and other parts, causing inflammation and tissue damage. At the same time, the dysfunction of T cells and NK cells can not effectively inhibit the activation of B cells and the continuation of autoimmune response.
In conclusion, the mechanism of morbidity in systemic lupus erythematosus is a complex process involving the interaction of multiple factors. These factors together lead to the abnormality of the immune system, which makes the body produce immune attack to its own tissues, thus causing a series of clinical signs and symptoms and tissue damage. It is of great significance to study the morbidity mechanism of systemic lupus erythematosus for the diagnosis, treatment and prevention of the disease.
