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Article: The role of interferon-gamma in lymphocytic thyroiditis: Its functional and pathological effect on human thyrocytes in culture

TitleThe role of interferon-gamma in lymphocytic thyroiditis: Its functional and pathological effect on human thyrocytes in culture
Authors
Keywordshuman thyrocytcs
interferon‐gamma
lymphocytic thyroiditis
ultrastructural changes
Issue Date1992
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEI
Citation
Clinical And Experimental Immunology, 1992, v. 87 n. 2, p. 261-265 How to Cite?
AbstractInterferon-gamma (IFN-γ) has been recognized to possess diverse non-immunological effects on epithelial cells such as cellular growth and differentiation. We have previously demonstrated that IFN-γ suppressed thyroid-stimulating hormone (TSH)-stimulated thyroglobulin (TG) synthesis in human thyrocytes through inhibition of TG gene transcription. To define the pathological mechanism involved in the action of IFN-γ, we studied the ultrastructural changes of human thyrocytes cultured in monolayer. Stimulation of the thyrocytes with TSH 10 mU/ml for 2 days resulted in marked increase in TG release into the medium. This was accompanied by elongation of microvilli, increase in follicles and acinar formation, increase in secretory granules and prominence of Golgi apparatus and rough-surfaced endoplasmic reticulum. Addition of IFN-γ (500 U/ml) resulted in marked degeneration with shrinkage of the cell membrane, vacuolation of cytoplasm, swollen mitochondria and presence of lysosomal granules. Co-culturing the thyrocytes with the IFN-γ and TSH resulted in suppression of the morphological responsiveness to TSH. There was also suppression of TSH-induced TG secretion. However, at 500 U/ml IFN-γ did not cause lysis of the thyrocytes as estimated by the cellular DNA content. Furthermore, binucleated cells were frequently encountered in those wells that were treated with IFN-γ for either 2 or 5 days. The findings suggest that IFN-γ resulted in de-differentiation and degeneration of the thyrocytes, which subsequently regained the growth potential and showed attempts at regeneration. This may explain why most patients with lymphocytic thyroiditis recover from the acute injury and do not suffer from permanent hypothyroidism.
Persistent Identifierhttp://hdl.handle.net/10722/161928
ISSN
2023 Impact Factor: 3.4
2023 SCImago Journal Rankings: 1.114
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKung, AWCen_US
dc.contributor.authorMa, Len_US
dc.contributor.authorLau, KSen_US
dc.date.accessioned2012-09-05T05:16:06Z-
dc.date.available2012-09-05T05:16:06Z-
dc.date.issued1992en_US
dc.identifier.citationClinical And Experimental Immunology, 1992, v. 87 n. 2, p. 261-265en_US
dc.identifier.issn0009-9104en_US
dc.identifier.urihttp://hdl.handle.net/10722/161928-
dc.description.abstractInterferon-gamma (IFN-γ) has been recognized to possess diverse non-immunological effects on epithelial cells such as cellular growth and differentiation. We have previously demonstrated that IFN-γ suppressed thyroid-stimulating hormone (TSH)-stimulated thyroglobulin (TG) synthesis in human thyrocytes through inhibition of TG gene transcription. To define the pathological mechanism involved in the action of IFN-γ, we studied the ultrastructural changes of human thyrocytes cultured in monolayer. Stimulation of the thyrocytes with TSH 10 mU/ml for 2 days resulted in marked increase in TG release into the medium. This was accompanied by elongation of microvilli, increase in follicles and acinar formation, increase in secretory granules and prominence of Golgi apparatus and rough-surfaced endoplasmic reticulum. Addition of IFN-γ (500 U/ml) resulted in marked degeneration with shrinkage of the cell membrane, vacuolation of cytoplasm, swollen mitochondria and presence of lysosomal granules. Co-culturing the thyrocytes with the IFN-γ and TSH resulted in suppression of the morphological responsiveness to TSH. There was also suppression of TSH-induced TG secretion. However, at 500 U/ml IFN-γ did not cause lysis of the thyrocytes as estimated by the cellular DNA content. Furthermore, binucleated cells were frequently encountered in those wells that were treated with IFN-γ for either 2 or 5 days. The findings suggest that IFN-γ resulted in de-differentiation and degeneration of the thyrocytes, which subsequently regained the growth potential and showed attempts at regeneration. This may explain why most patients with lymphocytic thyroiditis recover from the acute injury and do not suffer from permanent hypothyroidism.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEIen_US
dc.relation.ispartofClinical and Experimental Immunologyen_US
dc.subjecthuman thyrocytcs-
dc.subjectinterferon‐gamma-
dc.subjectlymphocytic thyroiditis-
dc.subjectultrastructural changes-
dc.subject.meshCells, Cultureden_US
dc.subject.meshHumansen_US
dc.subject.meshInterferon-Gamma - Physiologyen_US
dc.subject.meshMicroscopy, Electronen_US
dc.subject.meshMicrovilli - Ultrastructureen_US
dc.subject.meshThyroglobulin - Biosynthesisen_US
dc.subject.meshThyroid Gland - Ultrastructureen_US
dc.subject.meshThyroiditis - Pathology - Physiopathologyen_US
dc.subject.meshThyrotropin - Pharmacologyen_US
dc.titleThe role of interferon-gamma in lymphocytic thyroiditis: Its functional and pathological effect on human thyrocytes in cultureen_US
dc.typeArticleen_US
dc.identifier.emailKung, AWC:awckung@hku.hken_US
dc.identifier.authorityKung, AWC=rp00368en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid1735190-
dc.identifier.scopuseid_2-s2.0-0026556878en_US
dc.identifier.volume87en_US
dc.identifier.issue2en_US
dc.identifier.spage261en_US
dc.identifier.epage265en_US
dc.identifier.isiWOS:A1992HB65100017-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridKung, AWC=7102322339en_US
dc.identifier.scopusauthoridMa, L=7403574642en_US
dc.identifier.scopusauthoridLau, KS=35205833900en_US
dc.identifier.issnl0009-9104-

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