Immunological Aspects of Graves’ Ophthalmopathy
The body’s autoimmune process is involved in the development of Graves’ disease (GD), which is manifested by an overactive thyroid gland. In some patients, autoreactive inflammatory reactions contribute to the development of symptoms such as thyroid ophthalmopathy, and the subsequent signs and sympt...
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| Veröffentlicht in: | BioMed research international 2019, Vol.2019 (2019), p.1-12 |
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| creator | Szczepanski, Miroslaw J. Mirza, Shafaq M. Kantor, Ireneusz Struga, Maria Nowicka, Grażyna Głuszko, Alicja Miśkiewicz, Piotr Łacheta, Dominika Poślednik, Krzysztof B. |
| description | The body’s autoimmune process is involved in the development of Graves’ disease (GD), which is manifested by an overactive thyroid gland. In some patients, autoreactive inflammatory reactions contribute to the development of symptoms such as thyroid ophthalmopathy, and the subsequent signs and symptoms are derived from the expansion of orbital adipose tissue and edema of extraocular muscles within the orbit. The autoimmune process, production of antibodies against self-antigens such as TSH receptor (TSHR) and IGF-1 receptor (IGF-1R), inflammatory infiltration, and accumulation of glycosaminoglycans (GAG) lead to edematous-infiltrative changes in periocular tissues. As a consequence, edema exophthalmos develops. Orbital fibroblasts seem to play a crucial role in orbital inflammation, tissue expansion, remodeling, and fibrosis because of their proliferative activity as well as their capacity to differentiate into adipocytes and myofibroblasts and production of GAG. In this paper, based on the available medical literature, the immunological mechanism of GO pathogenesis has been summarized. Particular attention was paid to the role of orbital fibroblasts and putative autoantigens. A deeper understanding of the pathomechanism of the disease and the involvement of immunological processes may give rise to the introduction of new, effective, and safe methods of treatment or monitoring of the disease activity. |
| doi_str_mv | 10.1155/2019/7453260 |
| format | Article |
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In some patients, autoreactive inflammatory reactions contribute to the development of symptoms such as thyroid ophthalmopathy, and the subsequent signs and symptoms are derived from the expansion of orbital adipose tissue and edema of extraocular muscles within the orbit. The autoimmune process, production of antibodies against self-antigens such as TSH receptor (TSHR) and IGF-1 receptor (IGF-1R), inflammatory infiltration, and accumulation of glycosaminoglycans (GAG) lead to edematous-infiltrative changes in periocular tissues. As a consequence, edema exophthalmos develops. Orbital fibroblasts seem to play a crucial role in orbital inflammation, tissue expansion, remodeling, and fibrosis because of their proliferative activity as well as their capacity to differentiate into adipocytes and myofibroblasts and production of GAG. In this paper, based on the available medical literature, the immunological mechanism of GO pathogenesis has been summarized. Particular attention was paid to the role of orbital fibroblasts and putative autoantigens. A deeper understanding of the pathomechanism of the disease and the involvement of immunological processes may give rise to the introduction of new, effective, and safe methods of treatment or monitoring of the disease activity.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2019/7453260</identifier><identifier>PMID: 31781640</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adipocytes ; Adipocytes - pathology ; Adipogenesis ; Adipose Tissue ; Adipose tissues ; Antibodies ; Antigens ; Autoantigens ; Autoantigens - immunology ; Autoimmunity ; B cells ; Biomedical research ; Cytokines ; Cytokines - metabolism ; Development and progression ; Diabetes ; Edema ; Endocrinology ; Fibroblasts ; Fibroblasts - immunology ; Fibroblasts - pathology ; Fibrosis ; Glycosaminoglycans ; Graves Ophthalmopathy - immunology ; Graves Ophthalmopathy - pathology ; Graves Ophthalmopathy - therapy ; Graves' disease ; Humans ; Hyaluronic Acid - metabolism ; Hyperthyroidism ; Immunoglobulins ; Immunology ; Inflammation ; Inflammation - immunology ; Insulin-like growth factor I ; Insulin-like growth factors ; Lymphocytes ; Medical treatment ; Metabolism ; Muscle Development ; Muscles ; Oculomotor Muscles ; Oculomotor system ; Orbit - pathology ; Pathogenesis ; Receptor, IGF Type 1 ; Receptors, Thyrotropin - immunology ; Review ; Rheumatoid arthritis ; Signs and symptoms ; Thyroid ; Thyroid gland ; Thyroid Gland - pathology ; Thyroid-stimulating hormone ; Thyroid-stimulating hormone receptors ; Viral antibodies</subject><ispartof>BioMed research international, 2019, Vol.2019 (2019), p.1-12</ispartof><rights>Copyright © 2019 Dominika Łacheta et al.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>Copyright © 2019 Dominika Łacheta et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Dominika Łacheta et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-f5dc6de9163ffd7d054b24732126b495d56b67cd68bbf577d383204a596c94653</citedby><cites>FETCH-LOGICAL-c565t-f5dc6de9163ffd7d054b24732126b495d56b67cd68bbf577d383204a596c94653</cites><orcidid>0000-0002-5206-137X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875285/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875285/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31781640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Pirozzi, Christopher J.</contributor><contributor>Christopher J Pirozzi</contributor><creatorcontrib>Szczepanski, Miroslaw J.</creatorcontrib><creatorcontrib>Mirza, Shafaq M.</creatorcontrib><creatorcontrib>Kantor, Ireneusz</creatorcontrib><creatorcontrib>Struga, Maria</creatorcontrib><creatorcontrib>Nowicka, Grażyna</creatorcontrib><creatorcontrib>Głuszko, Alicja</creatorcontrib><creatorcontrib>Miśkiewicz, Piotr</creatorcontrib><creatorcontrib>Łacheta, Dominika</creatorcontrib><creatorcontrib>Poślednik, Krzysztof B.</creatorcontrib><title>Immunological Aspects of Graves’ Ophthalmopathy</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>The body’s autoimmune process is involved in the development of Graves’ disease (GD), which is manifested by an overactive thyroid gland. In some patients, autoreactive inflammatory reactions contribute to the development of symptoms such as thyroid ophthalmopathy, and the subsequent signs and symptoms are derived from the expansion of orbital adipose tissue and edema of extraocular muscles within the orbit. The autoimmune process, production of antibodies against self-antigens such as TSH receptor (TSHR) and IGF-1 receptor (IGF-1R), inflammatory infiltration, and accumulation of glycosaminoglycans (GAG) lead to edematous-infiltrative changes in periocular tissues. As a consequence, edema exophthalmos develops. Orbital fibroblasts seem to play a crucial role in orbital inflammation, tissue expansion, remodeling, and fibrosis because of their proliferative activity as well as their capacity to differentiate into adipocytes and myofibroblasts and production of GAG. In this paper, based on the available medical literature, the immunological mechanism of GO pathogenesis has been summarized. Particular attention was paid to the role of orbital fibroblasts and putative autoantigens. A deeper understanding of the pathomechanism of the disease and the involvement of immunological processes may give rise to the introduction of new, effective, and safe methods of treatment or monitoring of the disease activity.</description><subject>Adipocytes</subject><subject>Adipocytes - pathology</subject><subject>Adipogenesis</subject><subject>Adipose Tissue</subject><subject>Adipose tissues</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Autoantigens</subject><subject>Autoantigens - immunology</subject><subject>Autoimmunity</subject><subject>B cells</subject><subject>Biomedical research</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Edema</subject><subject>Endocrinology</subject><subject>Fibroblasts</subject><subject>Fibroblasts - immunology</subject><subject>Fibroblasts - pathology</subject><subject>Fibrosis</subject><subject>Glycosaminoglycans</subject><subject>Graves Ophthalmopathy - immunology</subject><subject>Graves Ophthalmopathy - pathology</subject><subject>Graves Ophthalmopathy - therapy</subject><subject>Graves' disease</subject><subject>Humans</subject><subject>Hyaluronic Acid - metabolism</subject><subject>Hyperthyroidism</subject><subject>Immunoglobulins</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Inflammation - immunology</subject><subject>Insulin-like growth factor I</subject><subject>Insulin-like growth factors</subject><subject>Lymphocytes</subject><subject>Medical treatment</subject><subject>Metabolism</subject><subject>Muscle Development</subject><subject>Muscles</subject><subject>Oculomotor Muscles</subject><subject>Oculomotor system</subject><subject>Orbit - pathology</subject><subject>Pathogenesis</subject><subject>Receptor, IGF Type 1</subject><subject>Receptors, Thyrotropin - immunology</subject><subject>Review</subject><subject>Rheumatoid arthritis</subject><subject>Signs and symptoms</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroid Gland - pathology</subject><subject>Thyroid-stimulating hormone</subject><subject>Thyroid-stimulating hormone receptors</subject><subject>Viral antibodies</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkc1O3DAUhS1UBAjYsa5GYlOpneLf62SDNEItjITEBtaW459JUBKHOAGx62v09fokdTTDTMuKu7lX8qdz7_FB6Izg74QIcUExyS8kF4wC3kNHlBE-B8LJp-3M2CE6jfERp8oI4BwO0CEjMs0cHyGybJqxDXVYVUbXs0XsnBniLPjZda-fXfzz6_fsriuHUtdN6PRQvp6gfa_r6E43_Rg9_Pxxf3Uzv727Xl4tbudGgBjmXlgD1uUEmPdWWix4QblklFAoeC6sgAKksZAVhRdSWpYxirkWOZicg2DH6HKt241F46xx7dDrWnV91ej-VQVdqf9f2qpUq_CsIJOCZpPAl41AH55GFwfVVNG4utatC2NUNO1jEiiHhJ6_Qx_D2LfJXqKmv-JZRnfUStdOVa0Paa-ZRNUCkq2cZTBR39aU6UOMvfPbkwlWU2hqCk1tQkv4539tbuG3iBLwdQ2UVWv1S_VBOZcY5_WOJlQyTNhf94umkQ</recordid><startdate>2019</startdate><enddate>2019</enddate><creator>Szczepanski, Miroslaw J.</creator><creator>Mirza, Shafaq M.</creator><creator>Kantor, Ireneusz</creator><creator>Struga, Maria</creator><creator>Nowicka, Grażyna</creator><creator>Głuszko, Alicja</creator><creator>Miśkiewicz, Piotr</creator><creator>Łacheta, Dominika</creator><creator>Poślednik, Krzysztof B.</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5206-137X</orcidid></search><sort><creationdate>2019</creationdate><title>Immunological Aspects of Graves’ Ophthalmopathy</title><author>Szczepanski, Miroslaw J. ; Mirza, Shafaq M. ; Kantor, Ireneusz ; Struga, Maria ; Nowicka, Grażyna ; Głuszko, Alicja ; Miśkiewicz, Piotr ; Łacheta, Dominika ; Poślednik, Krzysztof B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-f5dc6de9163ffd7d054b24732126b495d56b67cd68bbf577d383204a596c94653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adipocytes</topic><topic>Adipocytes - pathology</topic><topic>Adipogenesis</topic><topic>Adipose Tissue</topic><topic>Adipose tissues</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Autoantigens</topic><topic>Autoantigens - immunology</topic><topic>Autoimmunity</topic><topic>B cells</topic><topic>Biomedical research</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Edema</topic><topic>Endocrinology</topic><topic>Fibroblasts</topic><topic>Fibroblasts - immunology</topic><topic>Fibroblasts - pathology</topic><topic>Fibrosis</topic><topic>Glycosaminoglycans</topic><topic>Graves Ophthalmopathy - immunology</topic><topic>Graves Ophthalmopathy - pathology</topic><topic>Graves Ophthalmopathy - therapy</topic><topic>Graves' disease</topic><topic>Humans</topic><topic>Hyaluronic Acid - metabolism</topic><topic>Hyperthyroidism</topic><topic>Immunoglobulins</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Inflammation - immunology</topic><topic>Insulin-like growth factor I</topic><topic>Insulin-like growth factors</topic><topic>Lymphocytes</topic><topic>Medical treatment</topic><topic>Metabolism</topic><topic>Muscle Development</topic><topic>Muscles</topic><topic>Oculomotor Muscles</topic><topic>Oculomotor system</topic><topic>Orbit - pathology</topic><topic>Pathogenesis</topic><topic>Receptor, IGF Type 1</topic><topic>Receptors, Thyrotropin - immunology</topic><topic>Review</topic><topic>Rheumatoid arthritis</topic><topic>Signs and symptoms</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroid Gland - pathology</topic><topic>Thyroid-stimulating hormone</topic><topic>Thyroid-stimulating hormone receptors</topic><topic>Viral antibodies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Szczepanski, Miroslaw J.</creatorcontrib><creatorcontrib>Mirza, Shafaq M.</creatorcontrib><creatorcontrib>Kantor, Ireneusz</creatorcontrib><creatorcontrib>Struga, Maria</creatorcontrib><creatorcontrib>Nowicka, Grażyna</creatorcontrib><creatorcontrib>Głuszko, Alicja</creatorcontrib><creatorcontrib>Miśkiewicz, Piotr</creatorcontrib><creatorcontrib>Łacheta, Dominika</creatorcontrib><creatorcontrib>Poślednik, Krzysztof B.</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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In some patients, autoreactive inflammatory reactions contribute to the development of symptoms such as thyroid ophthalmopathy, and the subsequent signs and symptoms are derived from the expansion of orbital adipose tissue and edema of extraocular muscles within the orbit. The autoimmune process, production of antibodies against self-antigens such as TSH receptor (TSHR) and IGF-1 receptor (IGF-1R), inflammatory infiltration, and accumulation of glycosaminoglycans (GAG) lead to edematous-infiltrative changes in periocular tissues. As a consequence, edema exophthalmos develops. Orbital fibroblasts seem to play a crucial role in orbital inflammation, tissue expansion, remodeling, and fibrosis because of their proliferative activity as well as their capacity to differentiate into adipocytes and myofibroblasts and production of GAG. In this paper, based on the available medical literature, the immunological mechanism of GO pathogenesis has been summarized. Particular attention was paid to the role of orbital fibroblasts and putative autoantigens. A deeper understanding of the pathomechanism of the disease and the involvement of immunological processes may give rise to the introduction of new, effective, and safe methods of treatment or monitoring of the disease activity.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31781640</pmid><doi>10.1155/2019/7453260</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-5206-137X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes Adipocytes - pathology Adipogenesis Adipose Tissue Adipose tissues Antibodies Antigens Autoantigens Autoantigens - immunology Autoimmunity B cells Biomedical research Cytokines Cytokines - metabolism Development and progression Diabetes Edema Endocrinology Fibroblasts Fibroblasts - immunology Fibroblasts - pathology Fibrosis Glycosaminoglycans Graves Ophthalmopathy - immunology Graves Ophthalmopathy - pathology Graves Ophthalmopathy - therapy Graves' disease Humans Hyaluronic Acid - metabolism Hyperthyroidism Immunoglobulins Immunology Inflammation Inflammation - immunology Insulin-like growth factor I Insulin-like growth factors Lymphocytes Medical treatment Metabolism Muscle Development Muscles Oculomotor Muscles Oculomotor system Orbit - pathology Pathogenesis Receptor, IGF Type 1 Receptors, Thyrotropin - immunology Review Rheumatoid arthritis Signs and symptoms Thyroid Thyroid gland Thyroid Gland - pathology Thyroid-stimulating hormone Thyroid-stimulating hormone receptors Viral antibodies |
| title | Immunological Aspects of Graves’ Ophthalmopathy |
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