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Article: Development of a Murine Model of Autoimmune Thyroiditis Induced with Homologous Mouse Thyroid Peroxidase

TitleDevelopment of a Murine Model of Autoimmune Thyroiditis Induced with Homologous Mouse Thyroid Peroxidase
Authors
Issue Date2004
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2004, v. 145 n. 2, p. 809-816 How to Cite?
AbstractAutoimmune thyroid disease (AITD) is a common autoimmune disease. Thyroid peroxidase (TPO) is a well characterized autoantigen in AITD. Autoantibodies and autoreactive T lymphocytes to TPO are believed to play a major role in the pathogenesis of lymphocytic thyroiditis. To understand the pathogenic mechanisms of AITD and the role of TPO, we have established a mouse model of lymphocytic thyroiditis by immunizing C57Bl/6 (H-2b), CBA (H-2 k), and C57Bl/6 x CBA F1 mice with recombinant murine TPO (rmTPO) ectodomain comprising amino acid residue 1-837 produced in Escherichia coli. Mice were immunized with 30 μg purified ectodomain in complete Freund's adjuvant. Antibodies against rmTPO were detected in the serum of all mice from day 21 onward. Draining lymph node cells from rmTPO-immunized animals showed dose-dependent proliferation to TPO stimulation. Mice killed at d 50 and 90 revealed variable degrees of thyroiditis with infiltration of mononuclear cells and destruction of thyroid follicles. C57Bl/6 and the F1 mice, in comparison with CBA mice, showed a greater degree of thyroiditis. There was alack of correction between the intensity of thyroiditis and the anti-TPO response. Immunotyping of the thyroid cellular infiltrates showed predominantly CD4 + T cells and B220+ B cells but scanty CD8+ T cells. None of the control mice injected with the purified fusion partner developed anti-TPO antibodies and thyroiditis. In conclusion, a genuine autoimmune mouse model of lymphocytic thyroiditis was established using autologous mouse TPO. This new model induced with autologous TPO will lead to a better understanding of the mechanisms in destructive thyroiditis and will assist in the development of new strategies for modulating the pathogenic immune response.
Persistent Identifierhttp://hdl.handle.net/10722/77447
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNg, HPen_HK
dc.contributor.authorBanga, JPen_HK
dc.contributor.authorKung, AWCen_HK
dc.date.accessioned2010-09-06T07:32:00Z-
dc.date.available2010-09-06T07:32:00Z-
dc.date.issued2004en_HK
dc.identifier.citationEndocrinology, 2004, v. 145 n. 2, p. 809-816en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77447-
dc.description.abstractAutoimmune thyroid disease (AITD) is a common autoimmune disease. Thyroid peroxidase (TPO) is a well characterized autoantigen in AITD. Autoantibodies and autoreactive T lymphocytes to TPO are believed to play a major role in the pathogenesis of lymphocytic thyroiditis. To understand the pathogenic mechanisms of AITD and the role of TPO, we have established a mouse model of lymphocytic thyroiditis by immunizing C57Bl/6 (H-2b), CBA (H-2 k), and C57Bl/6 x CBA F1 mice with recombinant murine TPO (rmTPO) ectodomain comprising amino acid residue 1-837 produced in Escherichia coli. Mice were immunized with 30 μg purified ectodomain in complete Freund's adjuvant. Antibodies against rmTPO were detected in the serum of all mice from day 21 onward. Draining lymph node cells from rmTPO-immunized animals showed dose-dependent proliferation to TPO stimulation. Mice killed at d 50 and 90 revealed variable degrees of thyroiditis with infiltration of mononuclear cells and destruction of thyroid follicles. C57Bl/6 and the F1 mice, in comparison with CBA mice, showed a greater degree of thyroiditis. There was alack of correction between the intensity of thyroiditis and the anti-TPO response. Immunotyping of the thyroid cellular infiltrates showed predominantly CD4 + T cells and B220+ B cells but scanty CD8+ T cells. None of the control mice injected with the purified fusion partner developed anti-TPO antibodies and thyroiditis. In conclusion, a genuine autoimmune mouse model of lymphocytic thyroiditis was established using autologous mouse TPO. This new model induced with autologous TPO will lead to a better understanding of the mechanisms in destructive thyroiditis and will assist in the development of new strategies for modulating the pathogenic immune response.en_HK
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_HK
dc.relation.ispartofEndocrinologyen_HK
dc.rightsEndocrinology . Copyright © The Endocrine Society.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAutoantibodies - blooden_HK
dc.subject.meshCell Divisionen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshImmunizationen_HK
dc.subject.meshIodide Peroxidase - immunologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Inbred CBAen_HK
dc.subject.meshRecombinant Proteins - immunologyen_HK
dc.subject.meshT-Lymphocytes - pathologyen_HK
dc.subject.meshThyroid Gland - pathologyen_HK
dc.subject.meshThyroiditis, Autoimmune - blood - immunology - pathologyen_HK
dc.subject.meshThyroxine - blooden_HK
dc.titleDevelopment of a Murine Model of Autoimmune Thyroiditis Induced with Homologous Mouse Thyroid Peroxidaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0013-7227&volume=145&issue=2&spage=809&epage=16&date=2004&atitle=Development+of+a+murine+model+of+autoimmune+thyroiditis+induced+with+homologous+mouse+thyroid+peroxidaseen_HK
dc.identifier.emailKung, AWC:awckung@hku.hken_HK
dc.identifier.authorityKung, AWC=rp00368en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/en.2003-0656en_HK
dc.identifier.pmid14592961en_HK
dc.identifier.scopuseid_2-s2.0-0842291558en_HK
dc.identifier.hkuros87822en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0842291558&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume145en_HK
dc.identifier.issue2en_HK
dc.identifier.spage809en_HK
dc.identifier.epage816en_HK
dc.identifier.isiWOS:000188304400042-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNg, HP=14621713300en_HK
dc.identifier.scopusauthoridBanga, JP=7102475139en_HK
dc.identifier.scopusauthoridKung, AWC=7102322339en_HK

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