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Article: Effects of interferon-γ therapy on thyroid function, T-lymphocyte subpopulations and induction of autoantibodies

TitleEffects of interferon-γ therapy on thyroid function, T-lymphocyte subpopulations and induction of autoantibodies
Authors
Issue Date1990
PublisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
Citation
Journal Of Clinical Endocrinology And Metabolism, 1990, v. 71 n. 5, p. 1230-1234 How to Cite?
AbstractTreatment with human leucocyte interferon (IFNα) has been associated with the development of thyroid autoimmunity and hypothyroidism, but it is not certain whether this phenomenon was a result of contamination with IFNγ, which induced HLA class II antigen expression on T-lymphocytes. We prospectively studied 11 subjects (5 females and 6 males; mean age, 26.8 yr; range, 18-36) with chronic active hepatitis B who were randomized to receive recombinant human IFNγ (rhIFNγ; 106 U/m2·day, im, 3 times/week) for 16 weeks. Goiter was not present, and no patient had a history or family history of autoimmune diseases. Serial thyroid functions, including serum T4, T3, free thyroid hormone index, free T4 and TSH before, during, and on subsequent follow-up for a period of 1 yr were all normal. Eight patients had adequate serial samples for study of serological and lymphocyte subpopulations. None of the patients treated with rhIFNγ developed thyroglobulin or thyroid microsomal antibodies. However, four patients developed antinuclear and smooth muscle autoantibodies during or after rhIFNγ treatment. Treatment with rhIFNγ resulted in a significant increase in circulating T-lymphocytes and HLA-DR-positive T-cells (P < 0.05), with equal proportions of circulating CD4+ and CD8+ T-cells becoming DR positive. The percentage of HLA-DR-positive T-cells remained elevated after discontinuation of rhIFNγ. Also, rhIFNγ treatment led to a decrease in the number of circulating granulocytes and interleukin-2 receptor-positive cells. In conclusion, we did not observe any thyroid dysfunction or thyroid autoimmunity in our patients treated with the studied dose of rhIFNγ, but induction of other autoantibodies was observed.
Persistent Identifierhttp://hdl.handle.net/10722/161820
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.940
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKung, AWCen_US
dc.contributor.authorJones, BMen_US
dc.contributor.authorLai, CLen_US
dc.date.accessioned2012-09-05T05:15:17Z-
dc.date.available2012-09-05T05:15:17Z-
dc.date.issued1990en_US
dc.identifier.citationJournal Of Clinical Endocrinology And Metabolism, 1990, v. 71 n. 5, p. 1230-1234en_US
dc.identifier.issn0021-972Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/161820-
dc.description.abstractTreatment with human leucocyte interferon (IFNα) has been associated with the development of thyroid autoimmunity and hypothyroidism, but it is not certain whether this phenomenon was a result of contamination with IFNγ, which induced HLA class II antigen expression on T-lymphocytes. We prospectively studied 11 subjects (5 females and 6 males; mean age, 26.8 yr; range, 18-36) with chronic active hepatitis B who were randomized to receive recombinant human IFNγ (rhIFNγ; 106 U/m2·day, im, 3 times/week) for 16 weeks. Goiter was not present, and no patient had a history or family history of autoimmune diseases. Serial thyroid functions, including serum T4, T3, free thyroid hormone index, free T4 and TSH before, during, and on subsequent follow-up for a period of 1 yr were all normal. Eight patients had adequate serial samples for study of serological and lymphocyte subpopulations. None of the patients treated with rhIFNγ developed thyroglobulin or thyroid microsomal antibodies. However, four patients developed antinuclear and smooth muscle autoantibodies during or after rhIFNγ treatment. Treatment with rhIFNγ resulted in a significant increase in circulating T-lymphocytes and HLA-DR-positive T-cells (P < 0.05), with equal proportions of circulating CD4+ and CD8+ T-cells becoming DR positive. The percentage of HLA-DR-positive T-cells remained elevated after discontinuation of rhIFNγ. Also, rhIFNγ treatment led to a decrease in the number of circulating granulocytes and interleukin-2 receptor-positive cells. In conclusion, we did not observe any thyroid dysfunction or thyroid autoimmunity in our patients treated with the studied dose of rhIFNγ, but induction of other autoantibodies was observed.en_US
dc.languageengen_US
dc.publisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.orgen_US
dc.relation.ispartofJournal of Clinical Endocrinology and Metabolismen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAntigens, Cd4 - Blooden_US
dc.subject.meshAntigens, Cd8en_US
dc.subject.meshAntigens, Differentiation, T-Lymphocyte - Blooden_US
dc.subject.meshAutoantibodies - Biosynthesisen_US
dc.subject.meshFemaleen_US
dc.subject.meshHla-Dr Antigens - Blooden_US
dc.subject.meshHepatitis B - Drug Therapy - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInterferon-Gamma - Adverse Effects - Therapeutic Useen_US
dc.subject.meshMaleen_US
dc.subject.meshRecombinant Proteins - Adverse Effectsen_US
dc.subject.meshT-Lymphocyte Subsets - Drug Effectsen_US
dc.subject.meshThyroid Function Testsen_US
dc.subject.meshThyroid Gland - Drug Effects - Physiologyen_US
dc.subject.meshThyroiditis, Autoimmune - Chemically Induceden_US
dc.titleEffects of interferon-γ therapy on thyroid function, T-lymphocyte subpopulations and induction of autoantibodiesen_US
dc.typeArticleen_US
dc.identifier.emailKung, AWC:awckung@hku.hken_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityKung, AWC=rp00368en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1210/jcem-71-5-1230-
dc.identifier.pmid2121769-
dc.identifier.scopuseid_2-s2.0-0025027271en_US
dc.identifier.volume71en_US
dc.identifier.issue5en_US
dc.identifier.spage1230en_US
dc.identifier.epage1234en_US
dc.identifier.isiWOS:A1990EF13200026-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridKung, AWC=7102322339en_US
dc.identifier.scopusauthoridJones, BM=7404958958en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US

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