Clinical evidence that connects HT with PTC is summarized and how these two conditions interact are examined, aiming to provide a theoretical foundation for developing personalized therapies that target the tumor immune microenvironment (TIME) during HT.
Abstract
The growing body of evidence suggests a complicated association between papillary thyroid cancer (PTC) and Hashimoto’s thyroiditis (HT). Although HT is a major risk factor for PTC development, it is also associated with improved patient outcomes. However, the molecular mechanisms between these two diseases remain unclear. This narrative review summarizes clinical evidence that connects HT with PTC and examines how these two conditions interact. It explores the involvement of CD4+ T-cell subsets, regulatory T cells, CD8+ T cells, tumor-associated macrophages, and key immunological molecules in remodeling the tumor immune microenvironment (TIME) during HT. We also discuss the contributions of genetic predisposition, environmental factors, thyroid-stimulating hormone and autoantibodies, non-coding RNA regulatory networks, and the gut microbiota to the relationship between the two diseases. Further research is needed to fill the gaps in our understanding of HT and PTC linkages, aiming to provide a theoretical foundation for developing personalized therapies that target the TIME.
Hashimoto's thyroiditis is the most common cause of primary hypothyroidism in iodine-sufficient regions and is characterised by immune-mediated injury to thyroid follicular cells. Its pathophysiology involves an interplay of genetic susceptibility, environmental exposures, and epigenetic modifications that disrupt immu...
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