Systemic lupus erythematosus (SLE) is an autoimmune disorder that affects over 250,000 people in the United States alone. 90% of the patients with SLE are female, which indicates that there is either an important role in female hormones or a protective role in male hormones. However, it is also possible that the gene is carried on the X chromosome, making males less likely to contract the disease (Rahman, et al. 929). Autoantibodies are generated in people with SLE, meaning that the humoral immunity system has lost the ability to differentiate between foreign and native self. The most common autoantibody, anti-dsDNA, binds to double-stranded DNA in the cells and tissues; however, there are also anti-nucleosome, anti-Rho, anti-NMDA, and other
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The most common autoantibody produced in SLE is anti-double stranded DNA; however, there are other possible antibodies, including, but not limited to, anti-Rho, anti-nucleosome, and anti-NMDA. Because all of these antibodies are present in varying concentrations, symptoms of SLE vary widely, making it difficult to diagnose. However, what all SLE patients have in common is that the B-cells have lost the ability to differentiate between foreign antigens and native self. Because the B-cells are the predominate issue, it makes sense to target B-cells as therapeutic agents. There are several different ways that researchers have attempted to target the B-cells. The first way is through B-cell surface antigens, which include CD19, CD20, and CD22. Targeting these surface proteins with antibodies ultimately leads to cell death, although the mechanism varies. However, these surface antigens are present on most B-cells, which prevents selective destruction of malfunctioning B-cells. Targeting growth factors for B-cells, BAFF and APRIL seems promising based on studies in mice; however, one can imagine that this would not selectively inhibit the growth of only malfunctioning B-cells, thus affecting the healthy immune system of a patient. There is a different cytokine, IL-6, that may inhibit growth of malfunctioning B-cells, making it a promising drug candidate for the future. Lastly, researchers have looked at targeting the B- and T-cell interaction to prevent the immune system from attacking itself in a more efficient manner. However, this is in early stages of development and only decreasing the amount of CD40L has been tested, not actually inhibiting the interaction between the B- and T-cells. Because SLE utilizes every part of the immune system to attack itself, it is very difficult to find one solution that will solve the entire problem. Hopefully in the future, specific genes can be identified
The most common autoantibody produced in SLE is anti-double stranded DNA; however, there are other possible antibodies, including, but not limited to, anti-Rho, anti-nucleosome, and anti-NMDA. Because all of these antibodies are present in varying concentrations, symptoms of SLE vary widely, making it difficult to diagnose. However, what all SLE patients have in common is that the B-cells have lost the ability to differentiate between foreign antigens and native self. Because the B-cells are the predominate issue, it makes sense to target B-cells as therapeutic agents. There are several different ways that researchers have attempted to target the B-cells. The first way is through B-cell surface antigens, which include CD19, CD20, and CD22. Targeting these surface proteins with antibodies ultimately leads to cell death, although the mechanism varies. However, these surface antigens are present on most B-cells, which prevents selective destruction of malfunctioning B-cells. Targeting growth factors for B-cells, BAFF and APRIL seems promising based on studies in mice; however, one can imagine that this would not selectively inhibit the growth of only malfunctioning B-cells, thus affecting the healthy immune system of a patient. There is a different cytokine, IL-6, that may inhibit growth of malfunctioning B-cells, making it a promising drug candidate for the future. Lastly, researchers have looked at targeting the B- and T-cell interaction to prevent the immune system from attacking itself in a more efficient manner. However, this is in early stages of development and only decreasing the amount of CD40L has been tested, not actually inhibiting the interaction between the B- and T-cells. Because SLE utilizes every part of the immune system to attack itself, it is very difficult to find one solution that will solve the entire problem. Hopefully in the future, specific genes can be identified