ER stress impairs MHC Class I surface expression and increases susceptibility of thyroid cells to NK-mediated cytotoxicity
| Autor: | Mariangela Annunziatella, Giuseppina Ruggiero, B. Di Jeso, Luca Ulianich, Giuseppe Terrazzano, Francesco Beguinot |
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| Přispěvatelé: | Ulianich, L, Terrazzano, G, Annunziatella, M, Ruggiero, G, Beguinot, F, DI JESO, Bruno, Ulianich, L., Terrazzano, G., Annunziatella, M., Ruggiero, Giuseppina, Beguinot, Francesco, Di Jeso, B. |
| Jazyk: | angličtina |
| Předmět: |
Cytotoxicity
Immunologic medicine.medical_specialty Cell type Thapsigargin MHC-I expression Natural killer cell Thyroid Gland Down-Regulation Gene Expression Endoplasmic Reticulum Major histocompatibility complex Cell Line Interferon-gamma 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine MHC class I Tumor Cells Cultured medicine Humans Cytotoxicity Molecular Biology Protein Unfolding 030304 developmental biology Thyroid autoimmunity ER stress Natural killer cells 0303 health sciences biology Tunicamycin Histocompatibility Antigens Class I 3. Good health Cell biology Killer Cells Natural immune system Endocrinology chemistry Cell culture 030220 oncology & carcinogenesis biology.protein Unfolded protein response thyroiditis Molecular Medicine ER stre |
| Zdroj: | Biochimica et biophysica acta. Molecular basis of disease 1812 (2011): 431–438. doi:10.1016/j.bbadis.2010.12.013 info:cnr-pdr/source/autori:Ulianich L, Terrazzano G, Annunziatella M, Ruggiero G, Beguinot F, Di Jeso B./titolo:ER stress impairs MHC Class I surface expression and increases susceptibility of thyroid cells to NK-mediated cytotoxicity./doi:10.1016%2Fj.bbadis.2010.12.013/rivista:Biochimica et biophysica acta. Molecular basis of disease/anno:2011/pagina_da:431/pagina_a:438/intervallo_pagine:431–438/volume:1812 |
| ISSN: | 0925-4439 |
| DOI: | 10.1016/j.bbadis.2010.12.013 |
| Popis: | We recently reported that, in thyroid cells, ER stress triggered by thapsigargin or tunicamycin, two well known ER stressing agents, induced dedifferentiation and loss of the epithelial phenotype in rat thyroid cells. In this study, we sought to evaluate if, in thyroid cells, ER stress could affect MHC class I expression and the possible implications of this effect in the alteration of function of natural killer cells, suggesting a role in thyroid pathology. In both, a human line of fetal thyroid cells (TAD-2 cells) and primary cultures of human thyroid cells, thapsigargin and tunicamicin triggered ER stress evaluated by BiP mRNA levels and XBP-1 splicing. In both cell types, TAD-2 cell line and primary cultures, major histocompatibility complex class I (MHC-I) plasmamembrane expression was significantly reduced by ER stress. This effect was accompanied by signs of natural killer activation. Thus, natural killer cells dramatically increased IFN-γ production and markedly increased their cytotoxicity against thyroid cells. Together, these data indicate that ER stress induces a decrease of MHC class I surface expression in thyroid cells, resulting in reduced natural killer-cell self-tolerance. |
| Databáze: | OpenAIRE |
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