Hashimoto's thyroiditis attenuates progression of papillary thyroid carcinoma: deciphering immunological links

Abstract

Although some studies have investigated the clinicopathologic relationships between papillary thyroid carcinoma (PTC) and Hashimoto's thyroiditis (HT), there is still no clear understanding of differences in tumor immune microenvironment for PTC with coexisting HT and HT effect on PTC progression. The aim of this study was to clarify immune-mediated mechanisms of coexisting HT, which might influence PTC progression. 30 patients with histologically confirmed conventional-type PTC and 30 patients with PTC and coexisting HT were enrolled in the study. To analyze the role of immune-mediated links between PTC and HT, immunohistochemical investigation was conducted to count the number of different immune cells including T-cytotoxic cells (CD8), plasma cells (CD138), Treg cells (FOXP3), mast cells (MCT), and M2 macrophages (CD163). It was shown that despite the high number of immune cells in the intact thyroid tissues of PTC patients with coexisting HT there were no significant differences in M2 macrophages, mast cells and Treg counts inside PTC with or without HT. PTC with HT was associated with a higher number of CD8þ cells (P < 0.001) reflecting the ability of immune system to generate and recruit T-cytotoxic cells in tumor area, which can explain the protective effect of HT on PTC progression. Lymph node metastases development was associated with an increased number of mast cells, M2 macrophages and Treg along with a decreased plasma cells count regardless of coexisting HT. However, we did not find significant differences in T-cytotoxic cells quantity in node-positive and node-negative patients with or without HT, which encourages further investigation of immune escape mechanisms in PTC.

Synchronous Occurrence of Papillary Thyroid Carcinoma and Medullary Carcinoma in Hashimoto’s Thyroiditis and Multi Nodular Goiter Background

“…The authors reported the frequencies of PTC and undifferentiated thyroid cancer were 6% and 2%, respectively, among all patients (14). The possibility of concurrence of HT, PTC, and MTC depends on some gene rearrangements (5,6,9,13). Besides these synchronous occurrences, HT has been introduced as playing a protective role against PTC progression (15).…”

“…The source of this cancer is follicular thyroid cells and PTC is known as the seventh most common cancer among women and the secondfastest-growing tumor among men (1,4). The risk factors of PTC has been documented as exposure to ionizing radiation, female gender, smoking, obesity, dietary iodine excess, alcohol, dietary nitrates, diabetes, and genetic factors (5). PTC is related to exclusive mutations, including BRAF V600E, RAS, and chromosomal rearrangements leading to the expression of tyrosine kinase receptors such as RET, NTRK, and ALK (2).…”

Laringopharingeal Reflux Impacts Immune Microenvironment of Laryngeal Carcinoma

“…Рефлюкс асоційований зі зменшенням рН, зміною експресії карбоангідрази ІІІ і спричиняє розвиток запалення, що може сприяти пух линній трансформації та впливати на реалі зацію протипухлинної імунної відповіді [2,7,8]. Ключовими клітинами протипухлинного імунітету є Т-цитотоксичні лімфоцити (CD8 + ) [9,10]. Закономірно, що щільність інфільтрації пухлин CD8 + -лімфоцитами, позитивно корелює з виживаністю хворих на РГ [8,11].…”

“…Показано, що зростання щільності інфільтрації пухлини CD3 + -і CD8 + -лімфоцитами було асоційоване з покращенням прогнозу перебігу пухлинного процесу у пацієнтів з карциномами голови та шиї [14]. Також відомо, що попереднє запалення та лімфоїдна інфільтрація можуть впливати на прогноз та ефективність лікування хворих з іншою онкологічною патологією [4,10,14]. Виявлені в роботі морфологічні зміни при ЛФР є досить закономірними з огляду на рівень рН та дію ферментів.…”

Mechanism of Xiaoying Daotan decoction in treating Hashimoto’s thyroiditis based on the Notch/Treg/Th17 pathway

“…With changes in lifestyle and improvements in detection technology, the incidence of this disease has been increasing, and the age of onset is mainly 30-50 years of age, with significantly more women than men impacted by HT (men vs. women: 1:4-20) (3,4). Studies have shown that the prevalence of papillary thyroid cancer in HT patients is higher than that of the normal population, suggesting that HT may be a risk factor for thyroid cancer (5). Some scholars have even proposed that HT is a precancerous lesion of papillary thyroid cancer (6).…”