Abstract
Hashimoto’s Thyroiditis (HT) is a chronic condition where the immune system attacks the thyroid gland. A life-long persisting autoimmune condition that begins with inflammation leading to thyroid dysfunction. Our research focuses on the pivotal part of the process: T helper 17 (Th17) cells since HT usually focuses on the other immune cells. Our study reveals that Th17 and the cytokine IL-17 are responsible for the condition’s inflammatory cascade. Th17 cells become proactive, leading to excessive inflammation, which ultimately causes thyroid tissue damage in HT. These cells are pro-inflammatory as they produce IL-17, which recruits other immune cells and exacerbates tissue destruction. This balance between the Th-17 and the regulatory Treg or T cells normally responsible for keeping immune response in check gets disrupted in HT, causing a persistent attack on the immune system. Our findings in this paper highlight the importance of targeting the Th-17 and IL-17 pathways as a potential therapeutic strategy. When we shift our focus on these, we may be able to develop treatments that help manage the inflammation and prevent thyroid damage.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call