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.
Read full abstract