ETA2023 Poster Presentations Basic Thyroid Gland, Iodine & Autoimmunity Basic (9 abstracts)
Thyroid-Resident memory T-cells specific for SARS-COV-2 are enriched in patients with thyroid disorders related to covid-19
Elena Carelli 1 , Ylenia Silvestri 2 , Francesca Clemente 2 , Giorgia Moschetti 2 , Sara Maioli 3 , Alejandro Espadas de Aris 4 , Rosanna Torelli 4 , Elena Longhi 4 , Tullia De Feo 4 , Mario Salvi 5 , Giovanna Mantovani 6 , Maura Arosio 7 , Mauro Bombaci 2 , Elisa Pesce 2 , Renata Grifantini 8 , Sergio Abrignani 8 , Jens Geginat 8 & Ilaria Muller 6
1Istituto Nazionale Genetica Molecolare Romeo Ed Enrica Invernizzi, Autoimmunity Lab, Milano, Italy; 2Istituto Nazionale Genetica Molecolare Romeo Ed Enrica Invernizzi, Milan, Italy; 3Dipartimento DI Scienze Cliniche e DI Comunità, Università DI Milano, Milan, Italy; 4S.C. Trapianti Lombardia - Nitp, Fondazione Irccs Cà Granda Ospedale Maggiore Policlinico; 5Struttura Complessa Endocrinologia, Fondazione Irccs Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy; 6Struttura Complessa Endocrinologia, Fondazione Irccs Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy, Dipartimento DI Scienze Cliniche e DI Comunità, Università DI Milano, Milan, Italy; 7Dipartimento DI Scienze Cliniche e DI Comunità, Università DI Milano, Milan, Italy, Struttura Complessa Endocrinologia, Fondazione Irccs Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy; 8Istituto Nazionale Genetica Molecolare Romeo Ed Enrica Invernizzi, Milan, Italy, Dipartimento DI Scienze Cliniche e DI Comunità, Università DI Milano, Milan, Italy
Objectives: SARS CoV-2 infections have been associated with the onset of classic subacute thyroiditis (SAT) or atypical SAT, observed in 10-15% of patients hospitalized for severe COVID19 disease (COV-A-SAT) and characterized by absence of neck pain, mild thyrotoxicosis associated with non-thyroidal illness syndrome and thyroiditis-like areas which may persist in the thyroid gland up to 12 months following SARS-CoV-2 infection, despite normalization of thyroid function. Little is known about thyroid anti-viral immune responses and the aim of the study is to define the role of circulating and thyroid-resident T-cells in COV-A-SAT patients.
Methods: T-cells derived from peripheral blood and thyroid (by fine-needle aspiration) samples of 13 unvaccinated COV-A-SAT patients, 6 patients developing classic SAT following COVID19 vaccination and no previous SARS-CoV-2 infection (VAX SAT), 6 patients with ATD (3 spontaneous and 3 following COVID19 vaccination) and 15 COVID19-naïve healthy donors (HD) were analyzed by multi-dimensional flow cytometry, UMAP and DiffusionMap dimensionality reduction and FlowSOM clustering. SARS-COV2-specific T-cells were identified by cytokine production induced by SARS-COV2-derived peptides and with COVID peptide-loaded HLA multimers after HLA haplotyping.
Results: COV-A-SAT patients showed activated Th1 and cytotoxic CD4+ and CD8+ effector T cells four months post-infection, which acquired a quiescent memory phenotype after eight months. Anti SARS CoV-2-specific CD4+ and CD8+ T-cell responses were detectable in peripheral blood four months post-infection, but were reduced after eight months. CD4+ and CD8+ tissue-resident memory cells (TRM) were present in the thyroid gland of COV-A-SAT patients, and circulating CXCR3+T-cells were identified as their putative precursors. SARS-CoV-2-specific T-cells were enriched in the thyroid and acquired a TRM phenotype eight months post-infection. Thyroid-resident TRM cells were also found in VAX-SAT and ATD patients, but no HD. Interestingly, we observed that HLA DRB1*13 was significantly over-represented in the total cohort of 13 COV-A-SAT patients as compared to healthy haplotyped donors. Moreover, there was also a significantly more frequent expression of HLA-B*57, suggesting that they may represent a genetic risk factor to develop COV-A-SAT.
Conclusions: Patients with thyroid disorders induced by severe Covid-19, in particular COV-A-SAT patients, show a prolonged systemic anti-viral effector T-cell response and the generation of COVID19-specific TRM in the thyroid target tissue. Such prolonged immune response may be in part responsible for the persistence of thyroiditis-like areas up to 12 months. Thyroid-resident TRM cells seem involved in thyroid disorders, both COVID19 related or not. The association of COV-A-SAT with specific HLA haplotypes suggests a genetic predisposition and a key role for T-cells.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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