Th17 Cells: The Silent Architects of Hashimoto’s Thyroiditis

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.

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Publication Details

Journal
International Journal of Progressive Sciences and Technologies
Published
2024-08-30
DOI
https://doi.org/10.52155/ijpsat.v46.1.6523
Primary Topic
Autoimmune Neurological Disorders and Treatments
Type
article
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article

Th17 Cells: The Silent Architects of Hashimoto’s Thyroiditis

Ajai Kumar Pandey, Netra Agarwal, Savitran Eshwar, Sharon Philip Jain et al.
International Journal of Progressive Sciences and Technologies
Autoimmune Neurological Disorders and Treatments
article

Th17 Cells: The Silent Architects of Hashimoto’s Thyroiditis

Ajai Kumar Pandey, Netra Agarwal, Savitran Eshwar, Sharon Philip Jain, Apurva Abitkar
article en

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.

International Journal of Progressive Sciences and TechnologiesVol. 46(1)
Medical University of Lublin (PL), Government Medical College (IN), Government Medical College (IN), David Tvildiani Medical University (GE), Georgian National University SEU, Tbilisi State Medical University (GE)
Openalex Percentile: Top 64%
Autoimmune Neurological Disorders and Treatments
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