22 - The Cellular Processes Behind Rheumatoid Arthritis
Description/Abstract/Artist Statement
Rheumatoid arthritis (RA) is a systematic chronic autoimmune disorder that usually affects joints and can eventually lead to full-body problems. The condition occurs when the immune system targets self-tissues in the body, leading to chronic joint inflammation and damage to other organs. RA pathogenesis involves interactions between genetic, environmental, and cellular functions. Molecular signaling pathways, such as JAK-STAT, MAPK, PI3K-AKT, and NF-κB contribute to the inflammation and abnormal immune response associated with RA. Additionally, T cells, B cells, macrophages, and cytokines are immune cells that play pivotal roles in RA inflammation. A genetic component has been identified in making individuals more susceptible to developing RA.
The current medications used to treat RA target the immune cells and molecular signaling pathways involved in the disease to lessen symptoms and prevent the rapid progression of the disease. To create more effective drug therapy treatments and improve the current ones, the molecular pathways of RA need to be further understood. This paper will overview the pathophysiology of RA, focusing on cellular pathways and genetic components.
Faculty Advisor/Mentor
Dr. Isaura Simões
Faculty Advisor/Mentor Department
Biological Sciences
Presentation Type
Poster
Disciplines
Immune System Diseases
22 - The Cellular Processes Behind Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a systematic chronic autoimmune disorder that usually affects joints and can eventually lead to full-body problems. The condition occurs when the immune system targets self-tissues in the body, leading to chronic joint inflammation and damage to other organs. RA pathogenesis involves interactions between genetic, environmental, and cellular functions. Molecular signaling pathways, such as JAK-STAT, MAPK, PI3K-AKT, and NF-κB contribute to the inflammation and abnormal immune response associated with RA. Additionally, T cells, B cells, macrophages, and cytokines are immune cells that play pivotal roles in RA inflammation. A genetic component has been identified in making individuals more susceptible to developing RA.
The current medications used to treat RA target the immune cells and molecular signaling pathways involved in the disease to lessen symptoms and prevent the rapid progression of the disease. To create more effective drug therapy treatments and improve the current ones, the molecular pathways of RA need to be further understood. This paper will overview the pathophysiology of RA, focusing on cellular pathways and genetic components.