When toxic molecules enter, mature T‐cells, memory T‐cells, and B‐cells are activated by the infected body cells. At the same time, more T‐helper cells are activated by the antigens presented on the macrophage. Next, B‐cells secrete antibodies to inactivate the toxic molecules by attaching and binding to them. They are then killed by the Cytotoxic T‐cells. Some of the B‐cells and T‐cells remain and transform into memory cells so that B‐cells can turn into plasma cells and secrete antibodies rapidly in the re‐infection. (National Institute of Allergy and Infectious Diseases, 2003) Systemic lupus erythematosus is an example of chronic autoimmune disease and it leads the immune system to fail to distinguish pathogens from healthy cells. First, Lupus raises the number of plasma cells than the infected plasma cells secrete autoantibodies which are a type of antibodies against the body tissues and they are the main cause of autoimmune disease. Secondly, the excess amount of autoantibodies begins to against body tissues under the abnormal functioning of the lupus infected immune system (Mok, 2003). After that, the damaged body cells attempt to heal themselves so inflammation is triggered and it can turn …show more content…
One of the common medication is Benlysta. The working principle is by blocking the survival signal of B‐cells development in order to reduce the lupus‐infected B‐cells which as shown in figure 3. However there are some possible side effects as shown in figure 4 which the symptoms can be categorized as infections, heart problem and mental illnesses. To conclude, women, Caucasians, African Americans, and Hispanics have a higher potential risk for having systemic lupus erythematosus. However, we just have a rough concept of the pathogenesis of systemic lupus erythematosus. The four factors which have a possible relationship with systemic lupus erythematosus are the CK40 ligand, Epstein‐Barr virus, ultraviolet (UV) radiation and tobacco smoking. For the future study, more experiments should be conducted to certain the pathogenesis of SLE. Also, Brown et al (2010) proposed that systemic lupus erythematosus may associate with genetic variation so the research may focus on the genetic factor. In addition, for the drug investigation, the direction should put emphasis on how to lessen the side effects and reinforce the effectiveness for treating the symptoms of systemic lupus