The role of infiltrating macrophages in islet destruction and regrowth in a transgenic model
The expression of interferon-gamma (IFN-γ) in pancreatic β cells leads to a complex pathology that represents the processes of both islet destruction and islet regeneration. Inflammatory cells and the factors elicited from them participate in the development of pathology in this transgenic model. To...
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| Veröffentlicht in: | Journal of autoimmunity 1995-08, Vol.8 (4), p.483-492 |
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| container_end_page | 492 |
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| container_title | Journal of autoimmunity |
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| creator | Gu, Danling O'Reilly, Lorraine Molony, Leslie Cooke, Anne Sarvetnick, Nora |
| description | The expression of interferon-gamma (IFN-γ) in pancreatic β cells leads to a complex pathology that represents the processes of both islet destruction and islet regeneration. Inflammatory cells and the factors elicited from them participate in the development of pathology in this transgenic model. To dissect the role of infiltrating macrophages in these events, the monoclonal directed against the type 3 complement receptor (5C6) was utilized to inhibit the extravasation of macrophages. This was approached by treating transgenic mice with 5C6 for 3 or 4 months, starting from 5–7 days of age. The data presented in this report demonstrate that infiltrating macrophages are important in the observed induction of diabetes in our transgenic model. We also found that infiltrating macrophages did not play a major role in the observed proliferation and islet regeneration, but some interesting subtleties regarding the regulation of this proliferative process emerged. |
| doi_str_mv | 10.1016/0896-8411(95)90003-9 |
| format | Article |
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Inflammatory cells and the factors elicited from them participate in the development of pathology in this transgenic model. To dissect the role of infiltrating macrophages in these events, the monoclonal directed against the type 3 complement receptor (5C6) was utilized to inhibit the extravasation of macrophages. This was approached by treating transgenic mice with 5C6 for 3 or 4 months, starting from 5–7 days of age. The data presented in this report demonstrate that infiltrating macrophages are important in the observed induction of diabetes in our transgenic model. We also found that infiltrating macrophages did not play a major role in the observed proliferation and islet regeneration, but some interesting subtleties regarding the regulation of this proliferative process emerged.</description><identifier>ISSN: 0896-8411</identifier><identifier>EISSN: 1095-9157</identifier><identifier>DOI: 10.1016/0896-8411(95)90003-9</identifier><identifier>PMID: 7492345</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Animals ; Biological and medical sciences ; Cell Division - immunology ; Cell Movement - immunology ; Diabetes Mellitus, Type 1 - etiology ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Islets of Langerhans - immunology ; Islets of Langerhans - pathology ; Islets of Langerhans - physiology ; Macrophages - immunology ; Macrophages - physiology ; Male ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Regeneration - immunology</subject><ispartof>Journal of autoimmunity, 1995-08, Vol.8 (4), p.483-492</ispartof><rights>1995</rights><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-35739e8c5e93c3cd6606e06c5a9c34f874900a7c40254aac1858b87ca665aeba3</citedby><cites>FETCH-LOGICAL-c417t-35739e8c5e93c3cd6606e06c5a9c34f874900a7c40254aac1858b87ca665aeba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/0896841195900039$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3657948$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7492345$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gu, Danling</creatorcontrib><creatorcontrib>O'Reilly, Lorraine</creatorcontrib><creatorcontrib>Molony, Leslie</creatorcontrib><creatorcontrib>Cooke, Anne</creatorcontrib><creatorcontrib>Sarvetnick, Nora</creatorcontrib><title>The role of infiltrating macrophages in islet destruction and regrowth in a transgenic model</title><title>Journal of autoimmunity</title><addtitle>J Autoimmun</addtitle><description>The expression of interferon-gamma (IFN-γ) in pancreatic β cells leads to a complex pathology that represents the processes of both islet destruction and islet regeneration. Inflammatory cells and the factors elicited from them participate in the development of pathology in this transgenic model. To dissect the role of infiltrating macrophages in these events, the monoclonal directed against the type 3 complement receptor (5C6) was utilized to inhibit the extravasation of macrophages. This was approached by treating transgenic mice with 5C6 for 3 or 4 months, starting from 5–7 days of age. The data presented in this report demonstrate that infiltrating macrophages are important in the observed induction of diabetes in our transgenic model. We also found that infiltrating macrophages did not play a major role in the observed proliferation and islet regeneration, but some interesting subtleties regarding the regulation of this proliferative process emerged.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Division - immunology</subject><subject>Cell Movement - immunology</subject><subject>Diabetes Mellitus, Type 1 - etiology</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Islets of Langerhans - immunology</subject><subject>Islets of Langerhans - pathology</subject><subject>Islets of Langerhans - physiology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Transgenic</subject><subject>Regeneration - immunology</subject><issn>0896-8411</issn><issn>1095-9157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE2LFDEURYMoY8_oP1DIQkQXpS-T740gg6PCgJtxJ4T0q1fdkapKm1Qr_nvTdtNLXb3FPfdxOYw9E_BGgDBvwXnTOSXEK69fewCQnX_AVgK87rzQ9iFbnZHH7LLW7wBCaK0v2IVV_loqvWLf7rfESx6J54GneUjjUuKS5g2fIpa828YN1RbwVEdaeE91KXtcUp55nHteaFPyr2V7ICJv1bluaE7Ip9zT-IQ9GuJY6enpXrGvtx_ubz51d18-fr55f9ehEnbppLbSk0NNXqLE3hgwBAZ19CjV4NpYgGhRwbVWMaJw2q2dxWiMjrSO8oq9PP7dlfxj3yaGKVWkcYwz5X0N1hoHYPR_QWHBWKlVA9URbA5qLTSEXUlTLL-DgHCwHw5qw0Ft8Dr8tR98qz0__d-vJ-rPpZPulr845bFiHIfmC1M9Y9Jo65Vr2LsjRk3az0QlVEw0I_WpEC6hz-nfO_4A0lugqQ</recordid><startdate>19950801</startdate><enddate>19950801</enddate><creator>Gu, Danling</creator><creator>O'Reilly, Lorraine</creator><creator>Molony, Leslie</creator><creator>Cooke, Anne</creator><creator>Sarvetnick, Nora</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19950801</creationdate><title>The role of infiltrating macrophages in islet destruction and regrowth in a transgenic model</title><author>Gu, Danling ; O'Reilly, Lorraine ; Molony, Leslie ; Cooke, Anne ; Sarvetnick, Nora</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-35739e8c5e93c3cd6606e06c5a9c34f874900a7c40254aac1858b87ca665aeba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Division - immunology</topic><topic>Cell Movement - immunology</topic><topic>Diabetes Mellitus, Type 1 - etiology</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Islets of Langerhans - immunology</topic><topic>Islets of Langerhans - pathology</topic><topic>Islets of Langerhans - physiology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Transgenic</topic><topic>Regeneration - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gu, Danling</creatorcontrib><creatorcontrib>O'Reilly, Lorraine</creatorcontrib><creatorcontrib>Molony, Leslie</creatorcontrib><creatorcontrib>Cooke, Anne</creatorcontrib><creatorcontrib>Sarvetnick, Nora</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of autoimmunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gu, Danling</au><au>O'Reilly, Lorraine</au><au>Molony, Leslie</au><au>Cooke, Anne</au><au>Sarvetnick, Nora</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of infiltrating macrophages in islet destruction and regrowth in a transgenic model</atitle><jtitle>Journal of autoimmunity</jtitle><addtitle>J Autoimmun</addtitle><date>1995-08-01</date><risdate>1995</risdate><volume>8</volume><issue>4</issue><spage>483</spage><epage>492</epage><pages>483-492</pages><issn>0896-8411</issn><eissn>1095-9157</eissn><abstract>The expression of interferon-gamma (IFN-γ) in pancreatic β cells leads to a complex pathology that represents the processes of both islet destruction and islet regeneration. Inflammatory cells and the factors elicited from them participate in the development of pathology in this transgenic model. To dissect the role of infiltrating macrophages in these events, the monoclonal directed against the type 3 complement receptor (5C6) was utilized to inhibit the extravasation of macrophages. This was approached by treating transgenic mice with 5C6 for 3 or 4 months, starting from 5–7 days of age. The data presented in this report demonstrate that infiltrating macrophages are important in the observed induction of diabetes in our transgenic model. We also found that infiltrating macrophages did not play a major role in the observed proliferation and islet regeneration, but some interesting subtleties regarding the regulation of this proliferative process emerged.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>7492345</pmid><doi>10.1016/0896-8411(95)90003-9</doi><tpages>10</tpages></addata></record> |
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| ispartof | Journal of autoimmunity, 1995-08, Vol.8 (4), p.483-492 |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals Biological and medical sciences Cell Division - immunology Cell Movement - immunology Diabetes Mellitus, Type 1 - etiology Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Islets of Langerhans - immunology Islets of Langerhans - pathology Islets of Langerhans - physiology Macrophages - immunology Macrophages - physiology Male Medical sciences Mice Mice, Inbred BALB C Mice, Transgenic Regeneration - immunology |
| title | The role of infiltrating macrophages in islet destruction and regrowth in a transgenic model |
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