Systemic lupus erythematosus (SLE) is an autoimmune disease caused by the immune system that attacks healthy tissues in the body. More than 50% of patients with SLE develop permanent organ damage caused by disease or existing treatments, which exacerbates disease-related symptoms and increases the risk of death. At least 5 million people worldwide suffer from some form of lupus. Today's top scientific journal nature published a study, northwestern university (Northwestern University) school of medicine and brghen women's hospital (Brigham and Women's Hospital) scientists led by the research team found a new target for SLE, for this target is developed to be expected in the reversal of SLE symptoms at the same time, avoid the overall inhibition of potential side effects of the immune system.
In this study, the scientists reported a new signaling pathway that drives lupus disease. Multiple molecules in the blood of lupus patients undergo disease-related changes. Ultimately, these changes result in insufficient activation of signaling pathways mediated by the aromatic hydrocarbon receptor (aryl hydrocarbon receptor, AHR) that regulates the response of immune cells to environmental contaminants, bacteria, or metabolites. Inadequate AHR activation leads to the production of excessive peripheral helper T cells that promote the production of pathogenic autoantibodies, leading to SLE disease or worsened symptoms.
Activation of AHR receptors promotes the proliferation of IL-22-releasing T cells (Th 22), which may accelerate the healing of SLE-induced damage. Simultaneous activation of the AHR receptor reduces the production of the chemokine CXCL13 that induces B cell migration, which may prevent autoantibody-releasing B cells from migration into healthy tissue to attack healthy tissue.
▲ Signaling pathways regulating the generation of IL-22-expressing T cells and peripheral helper T cells (Photo source: Reference [3])
To demonstrate that this discovery could be used to develop new drugs for SLE, the researchers reintroduced aromatic hydrocarbon receptor-activating molecules into the blood of lupus patients. The experimental results showed that this could reprogram the lupus-inducing cells into Th 22 cells to promote wound healing.
Co-corresponding author of the paper, dermatologist Dr. Jaehyuk Choi, Northwestern University School of Medicine, stated in a press release that current treatments for SLE are based on extensive immunosuppression. Development strategies to target AHR may produce more precise SLE therapies that can reverse SLE symptoms while avoiding the potential side effects of widespread immunosuppression. The research team is currently exploring ways to safely and effectively deliver AHR activating molecules into the human body.
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