Immune cell trafficking to the islets during type 1 diabetes
Summary Inhibition of immune cell trafficking to the pancreatic islets during type 1 diabetes (T1D) has therapeutic potential, since targeting of T cell and B cell trafficking has been clinically effective in other autoimmune diseases. Trafficking to the islets is characterized by redundancy in adhe...
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| Veröffentlicht in: | Clinical and experimental immunology 2019-12, Vol.198 (3), p.314-325 |
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| creator | Sandor, A. M. Jacobelli, J. Friedman, R. S. |
| description | Summary
Inhibition of immune cell trafficking to the pancreatic islets during type 1 diabetes (T1D) has therapeutic potential, since targeting of T cell and B cell trafficking has been clinically effective in other autoimmune diseases. Trafficking to the islets is characterized by redundancy in adhesion molecule and chemokine usage, which has not enabled effective targeting to date. Additionally, cognate antigen is not consistently required for T cell entry into the islets throughout the progression of disease. However, myeloid cells are required to enable T cell and B cell entry into the islets, and may serve as a convergence point in the pathways controlling this process. In this review we describe current knowledge of the factors that mediate immune cell trafficking to pancreatic islets during T1D progression.
Immune cell migration to the pancreatic islets during type 1 diabetes occurs by transendothelial migration, through a series of steps including rolling, arrest, and crawling on the vascular wall culminating with diapedesis through the endothelial barrier. Migration to the islets is characterized by redundancy in adhesion molecule and chemokine usage, and variable requirement for cognate antigen. However, myeloid cells are required to enable T cell and B cell entry into the islets and may serve as a convergence point in the pathways controlling this process. |
| doi_str_mv | 10.1111/cei.13353 |
| format | Article |
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Inhibition of immune cell trafficking to the pancreatic islets during type 1 diabetes (T1D) has therapeutic potential, since targeting of T cell and B cell trafficking has been clinically effective in other autoimmune diseases. Trafficking to the islets is characterized by redundancy in adhesion molecule and chemokine usage, which has not enabled effective targeting to date. Additionally, cognate antigen is not consistently required for T cell entry into the islets throughout the progression of disease. However, myeloid cells are required to enable T cell and B cell entry into the islets, and may serve as a convergence point in the pathways controlling this process. In this review we describe current knowledge of the factors that mediate immune cell trafficking to pancreatic islets during T1D progression.
Immune cell migration to the pancreatic islets during type 1 diabetes occurs by transendothelial migration, through a series of steps including rolling, arrest, and crawling on the vascular wall culminating with diapedesis through the endothelial barrier. Migration to the islets is characterized by redundancy in adhesion molecule and chemokine usage, and variable requirement for cognate antigen. However, myeloid cells are required to enable T cell and B cell entry into the islets and may serve as a convergence point in the pathways controlling this process.</description><identifier>ISSN: 0009-9104</identifier><identifier>ISSN: 1365-2249</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/cei.13353</identifier><identifier>PMID: 31343073</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>adhesion molecules ; Animals ; Autoimmune diseases ; autoimmunity ; B-Lymphocytes - immunology ; Beta cells ; Cell Movement - immunology ; cell trafficking ; Chemokines ; Diabetes ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Type 1 - immunology ; Diabetes Mellitus, Type 1 - pathology ; Disease Progression ; Humans ; Immunology of Diabetes Society Review Series: Insights into Pathogenesis of Type 1 Diabetes Series Editors: F. Susan Wong and Timothy I. Tree ; Islets of Langerhans - immunology ; Lymphocytes ; Lymphocytes T ; Myeloid cells ; Myeloid Cells - immunology ; Pancreas ; Pathogens ; Review ; Signal Transduction - immunology ; T-Lymphocytes - immunology</subject><ispartof>Clinical and experimental immunology, 2019-12, Vol.198 (3), p.314-325</ispartof><rights>2019 British Society for Immunology</rights><rights>2019 British Society for Immunology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4433-cb06ab9399c7d4fcdc2b7c4fe5fd047e10699a8f33e8417214d0151eb21c4b7a3</citedby><cites>FETCH-LOGICAL-c4433-cb06ab9399c7d4fcdc2b7c4fe5fd047e10699a8f33e8417214d0151eb21c4b7a3</cites><orcidid>0000-0001-7549-6387</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/PMC6857188/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6857188/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31343073$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sandor, A. M.</creatorcontrib><creatorcontrib>Jacobelli, J.</creatorcontrib><creatorcontrib>Friedman, R. S.</creatorcontrib><title>Immune cell trafficking to the islets during type 1 diabetes</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
Inhibition of immune cell trafficking to the pancreatic islets during type 1 diabetes (T1D) has therapeutic potential, since targeting of T cell and B cell trafficking has been clinically effective in other autoimmune diseases. Trafficking to the islets is characterized by redundancy in adhesion molecule and chemokine usage, which has not enabled effective targeting to date. Additionally, cognate antigen is not consistently required for T cell entry into the islets throughout the progression of disease. However, myeloid cells are required to enable T cell and B cell entry into the islets, and may serve as a convergence point in the pathways controlling this process. In this review we describe current knowledge of the factors that mediate immune cell trafficking to pancreatic islets during T1D progression.
Immune cell migration to the pancreatic islets during type 1 diabetes occurs by transendothelial migration, through a series of steps including rolling, arrest, and crawling on the vascular wall culminating with diapedesis through the endothelial barrier. Migration to the islets is characterized by redundancy in adhesion molecule and chemokine usage, and variable requirement for cognate antigen. However, myeloid cells are required to enable T cell and B cell entry into the islets and may serve as a convergence point in the pathways controlling this process.</description><subject>adhesion molecules</subject><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>autoimmunity</subject><subject>B-Lymphocytes - immunology</subject><subject>Beta cells</subject><subject>Cell Movement - immunology</subject><subject>cell trafficking</subject><subject>Chemokines</subject><subject>Diabetes</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes Mellitus, Type 1 - pathology</subject><subject>Disease Progression</subject><subject>Humans</subject><subject>Immunology of Diabetes Society Review Series: Insights into Pathogenesis of Type 1 Diabetes Series Editors: F. Susan Wong and Timothy I. Tree</subject><subject>Islets of Langerhans - immunology</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Myeloid cells</subject><subject>Myeloid Cells - immunology</subject><subject>Pancreas</subject><subject>Pathogens</subject><subject>Review</subject><subject>Signal Transduction - immunology</subject><subject>T-Lymphocytes - immunology</subject><issn>0009-9104</issn><issn>1365-2249</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctKAzEUhoMotlYXvoAMuNHFtDlJ5gYiSKlaENzoOmQyZ9rUudTJjNK3N71YVDCbkOTj4z_5CTkHOgS3RhrNEDgP-AHpAw8DnzGRHJI-pTTxE6CiR06sXbhjGIbsmPQ4cMFpxPvkZlqWXYWexqLw2kbludFvppp5be21c_SMLbC1XtY1m8vVEj3wMqNSbNGekqNcFRbPdvuAvN5PXsaP_tPzw3R89-RrITj3dUpDlSY8SXSUiVxnmqWRFjkGeUZFhEDDJFFxzjnGAiIGIqMQAKYMtEgjxQfkdutddmmJmcbKJS3ksjGlalayVkb-fqnMXM7qDxnGQQRx7ARXO0FTv3doW1kaux5ZVVh3VjIWc3A_yNbo5R90UXdN5caTjIMIgAWMOep6S-mmtrbBfB8GqFx3Il0nctOJYy9-pt-T3yU4YLQFPk2Bq_9NcjyZbpVfo_6U4Q</recordid><startdate>201912</startdate><enddate>201912</enddate><creator>Sandor, A. M.</creator><creator>Jacobelli, J.</creator><creator>Friedman, R. S.</creator><general>Oxford University Press</general><general>John Wiley and Sons Inc</general><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>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7549-6387</orcidid></search><sort><creationdate>201912</creationdate><title>Immune cell trafficking to the islets during type 1 diabetes</title><author>Sandor, A. M. ; Jacobelli, J. ; Friedman, R. S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4433-cb06ab9399c7d4fcdc2b7c4fe5fd047e10699a8f33e8417214d0151eb21c4b7a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>adhesion molecules</topic><topic>Animals</topic><topic>Autoimmune diseases</topic><topic>autoimmunity</topic><topic>B-Lymphocytes - immunology</topic><topic>Beta cells</topic><topic>Cell Movement - immunology</topic><topic>cell trafficking</topic><topic>Chemokines</topic><topic>Diabetes</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes Mellitus, Type 1 - pathology</topic><topic>Disease Progression</topic><topic>Humans</topic><topic>Immunology of Diabetes Society Review Series: Insights into Pathogenesis of Type 1 Diabetes Series Editors: F. Susan Wong and Timothy I. Tree</topic><topic>Islets of Langerhans - immunology</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Myeloid cells</topic><topic>Myeloid Cells - immunology</topic><topic>Pancreas</topic><topic>Pathogens</topic><topic>Review</topic><topic>Signal Transduction - immunology</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sandor, A. M.</creatorcontrib><creatorcontrib>Jacobelli, J.</creatorcontrib><creatorcontrib>Friedman, R. S.</creatorcontrib><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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sandor, A. M.</au><au>Jacobelli, J.</au><au>Friedman, R. S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immune cell trafficking to the islets during type 1 diabetes</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2019-12</date><risdate>2019</risdate><volume>198</volume><issue>3</issue><spage>314</spage><epage>325</epage><pages>314-325</pages><issn>0009-9104</issn><issn>1365-2249</issn><eissn>1365-2249</eissn><abstract>Summary
Inhibition of immune cell trafficking to the pancreatic islets during type 1 diabetes (T1D) has therapeutic potential, since targeting of T cell and B cell trafficking has been clinically effective in other autoimmune diseases. Trafficking to the islets is characterized by redundancy in adhesion molecule and chemokine usage, which has not enabled effective targeting to date. Additionally, cognate antigen is not consistently required for T cell entry into the islets throughout the progression of disease. However, myeloid cells are required to enable T cell and B cell entry into the islets, and may serve as a convergence point in the pathways controlling this process. In this review we describe current knowledge of the factors that mediate immune cell trafficking to pancreatic islets during T1D progression.
Immune cell migration to the pancreatic islets during type 1 diabetes occurs by transendothelial migration, through a series of steps including rolling, arrest, and crawling on the vascular wall culminating with diapedesis through the endothelial barrier. Migration to the islets is characterized by redundancy in adhesion molecule and chemokine usage, and variable requirement for cognate antigen. However, myeloid cells are required to enable T cell and B cell entry into the islets and may serve as a convergence point in the pathways controlling this process.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>31343073</pmid><doi>10.1111/cei.13353</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-7549-6387</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | adhesion molecules Animals Autoimmune diseases autoimmunity B-Lymphocytes - immunology Beta cells Cell Movement - immunology cell trafficking Chemokines Diabetes Diabetes mellitus (insulin dependent) Diabetes Mellitus, Type 1 - immunology Diabetes Mellitus, Type 1 - pathology Disease Progression Humans Immunology of Diabetes Society Review Series: Insights into Pathogenesis of Type 1 Diabetes Series Editors: F. Susan Wong and Timothy I. Tree Islets of Langerhans - immunology Lymphocytes Lymphocytes T Myeloid cells Myeloid Cells - immunology Pancreas Pathogens Review Signal Transduction - immunology T-Lymphocytes - immunology |
| title | Immune cell trafficking to the islets during type 1 diabetes |
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