Viewing Siglecs through the lens of tumor immunology
Summary Many Siglecs function as inhibitory receptors on innate and adaptive immune cells and may contribute to the attenuation of immune responses to tumors. Siglec 9 on neutrophils and Siglec 7 on NK cells are prominent examples of inhibitory Siglecs that can potentially dampen anti‐tumor immunity...
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| Veröffentlicht in: | Immunological reviews 2017-03, Vol.276 (1), p.178-191 |
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| container_title | Immunological reviews |
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| creator | Fraschilla, Isabella Pillai, Shiv |
| description | Summary
Many Siglecs function as inhibitory receptors on innate and adaptive immune cells and may contribute to the attenuation of immune responses to tumors. Siglec 9 on neutrophils and Siglec 7 on NK cells are prominent examples of inhibitory Siglecs that can potentially dampen anti‐tumor immunity. CD169 is a Siglec that may function as an adhesion molecule and a facilitator of the recognition and internalization of sialic acid decorated apoptotic bodies and exosomes derived from tumors. It can potentially contribute to both the attenuation as well as the facilitation of anti‐tumor immunity. Siglecs have been best studied in the tumor context in animal models of cancer. Modulators of Siglec function are likely to be developed and investigated clinically in a cancer context over the next few years. |
| doi_str_mv | 10.1111/imr.12526 |
| format | Article |
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Many Siglecs function as inhibitory receptors on innate and adaptive immune cells and may contribute to the attenuation of immune responses to tumors. Siglec 9 on neutrophils and Siglec 7 on NK cells are prominent examples of inhibitory Siglecs that can potentially dampen anti‐tumor immunity. CD169 is a Siglec that may function as an adhesion molecule and a facilitator of the recognition and internalization of sialic acid decorated apoptotic bodies and exosomes derived from tumors. It can potentially contribute to both the attenuation as well as the facilitation of anti‐tumor immunity. Siglecs have been best studied in the tumor context in animal models of cancer. Modulators of Siglec function are likely to be developed and investigated clinically in a cancer context over the next few years.</description><identifier>ISSN: 0105-2896</identifier><identifier>EISSN: 1600-065X</identifier><identifier>DOI: 10.1111/imr.12526</identifier><identifier>PMID: 28258691</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Adaptive Immunity ; Animal models ; Animals ; Antigens, CD - immunology ; Antigens, CD - metabolism ; Antigens, Differentiation, Myelomonocytic - immunology ; Antigens, Differentiation, Myelomonocytic - metabolism ; Apoptosis ; Attenuation ; Cancer ; cancer/tumor immunology ; Exosomes ; Humans ; hypersialylation ; immune evasion ; immune regulation ; Immune response ; Immune system ; Immunity ; Immunity, Innate ; Immunology ; Immunomodulation ; Immunotherapy - methods ; inhibitory receptor ; Internalization ; Killer Cells, Natural - immunology ; Lectins - immunology ; Lectins - metabolism ; Lenses ; Leukocytes (neutrophilic) ; Modulators ; Neoplasms - immunology ; Neoplasms - therapy ; Neutrophils - immunology ; Receptor mechanisms ; Receptors ; sialic acid ; Sialic Acid Binding Ig-like Lectin 1 - immunology ; Sialic Acid Binding Ig-like Lectin 1 - metabolism ; Sialic Acid Binding Immunoglobulin-like Lectins - immunology ; Sialic Acid Binding Immunoglobulin-like Lectins - metabolism ; Siglec ; Tumor Escape ; Tumors</subject><ispartof>Immunological reviews, 2017-03, Vol.276 (1), p.178-191</ispartof><rights>2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5426-f095062bb758a5a36dde5967a13332a5daa116cd869c6f767693b22bae8b58023</citedby><cites>FETCH-LOGICAL-c5426-f095062bb758a5a36dde5967a13332a5daa116cd869c6f767693b22bae8b58023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fimr.12526$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fimr.12526$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28258691$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fraschilla, Isabella</creatorcontrib><creatorcontrib>Pillai, Shiv</creatorcontrib><title>Viewing Siglecs through the lens of tumor immunology</title><title>Immunological reviews</title><addtitle>Immunol Rev</addtitle><description>Summary
Many Siglecs function as inhibitory receptors on innate and adaptive immune cells and may contribute to the attenuation of immune responses to tumors. Siglec 9 on neutrophils and Siglec 7 on NK cells are prominent examples of inhibitory Siglecs that can potentially dampen anti‐tumor immunity. CD169 is a Siglec that may function as an adhesion molecule and a facilitator of the recognition and internalization of sialic acid decorated apoptotic bodies and exosomes derived from tumors. It can potentially contribute to both the attenuation as well as the facilitation of anti‐tumor immunity. Siglecs have been best studied in the tumor context in animal models of cancer. Modulators of Siglec function are likely to be developed and investigated clinically in a cancer context over the next few years.</description><subject>Adaptive Immunity</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antigens, CD - immunology</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, Differentiation, Myelomonocytic - immunology</subject><subject>Antigens, Differentiation, Myelomonocytic - metabolism</subject><subject>Apoptosis</subject><subject>Attenuation</subject><subject>Cancer</subject><subject>cancer/tumor immunology</subject><subject>Exosomes</subject><subject>Humans</subject><subject>hypersialylation</subject><subject>immune evasion</subject><subject>immune regulation</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Immunity, Innate</subject><subject>Immunology</subject><subject>Immunomodulation</subject><subject>Immunotherapy - methods</subject><subject>inhibitory receptor</subject><subject>Internalization</subject><subject>Killer Cells, Natural - immunology</subject><subject>Lectins - immunology</subject><subject>Lectins - metabolism</subject><subject>Lenses</subject><subject>Leukocytes (neutrophilic)</subject><subject>Modulators</subject><subject>Neoplasms - immunology</subject><subject>Neoplasms - therapy</subject><subject>Neutrophils - immunology</subject><subject>Receptor mechanisms</subject><subject>Receptors</subject><subject>sialic acid</subject><subject>Sialic Acid Binding Ig-like Lectin 1 - immunology</subject><subject>Sialic Acid Binding Ig-like Lectin 1 - metabolism</subject><subject>Sialic Acid Binding Immunoglobulin-like Lectins - immunology</subject><subject>Sialic Acid Binding Immunoglobulin-like Lectins - metabolism</subject><subject>Siglec</subject><subject>Tumor Escape</subject><subject>Tumors</subject><issn>0105-2896</issn><issn>1600-065X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1LwzAYx4Mobk4PfgEpeNFDXZImaXIRZPgGiuAb3kLapl1G28xkdezbm7kpKgjm8hzy4_e8_AHYR_AEhTc0jTtBmGK2AfqIQRhDRl82QR8iSGPMBeuBHe8nEKI0wWQb9DDHlDOB-oA8Gz03bRU9mKrWuY9mY2e7ahyqjmrd-siW0axrrItM03StrW212AVbpaq93lvXAXi6OH8cXcU3d5fXo7ObOKcEs7iEgkKGsyylXFGVsKLQVLBUoSRJsKKFUgixvAiT5KxMWcpEkmGcKc0zyiFOBuB05Z12WaOLXLczp2o5daZRbiGtMvLnT2vGsrJvMiwHWSKC4GgtcPa1034mG-NzXdeq1bbzEvE05UgwQv-DEkJoSlhAD3-hE9u5NlxCIoEh4ULQZe_jFZU7673T5dfcCMplbDLEJj9iC-zB90W_yM-cAjBcAXNT68XfJnl9e79SvgMvH6Bj</recordid><startdate>201703</startdate><enddate>201703</enddate><creator>Fraschilla, Isabella</creator><creator>Pillai, Shiv</creator><general>Wiley Subscription Services, 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>7QL</scope><scope>7T5</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201703</creationdate><title>Viewing Siglecs through the lens of tumor immunology</title><author>Fraschilla, Isabella ; Pillai, Shiv</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5426-f095062bb758a5a36dde5967a13332a5daa116cd869c6f767693b22bae8b58023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adaptive Immunity</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antigens, CD - immunology</topic><topic>Antigens, CD - metabolism</topic><topic>Antigens, Differentiation, Myelomonocytic - immunology</topic><topic>Antigens, Differentiation, Myelomonocytic - metabolism</topic><topic>Apoptosis</topic><topic>Attenuation</topic><topic>Cancer</topic><topic>cancer/tumor immunology</topic><topic>Exosomes</topic><topic>Humans</topic><topic>hypersialylation</topic><topic>immune evasion</topic><topic>immune regulation</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Immunity, Innate</topic><topic>Immunology</topic><topic>Immunomodulation</topic><topic>Immunotherapy - methods</topic><topic>inhibitory receptor</topic><topic>Internalization</topic><topic>Killer Cells, Natural - immunology</topic><topic>Lectins - immunology</topic><topic>Lectins - metabolism</topic><topic>Lenses</topic><topic>Leukocytes (neutrophilic)</topic><topic>Modulators</topic><topic>Neoplasms - immunology</topic><topic>Neoplasms - therapy</topic><topic>Neutrophils - immunology</topic><topic>Receptor mechanisms</topic><topic>Receptors</topic><topic>sialic acid</topic><topic>Sialic Acid Binding Ig-like Lectin 1 - immunology</topic><topic>Sialic Acid Binding Ig-like Lectin 1 - metabolism</topic><topic>Sialic Acid Binding Immunoglobulin-like Lectins - immunology</topic><topic>Sialic Acid Binding Immunoglobulin-like Lectins - metabolism</topic><topic>Siglec</topic><topic>Tumor Escape</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fraschilla, Isabella</creatorcontrib><creatorcontrib>Pillai, Shiv</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</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>Immunological reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fraschilla, Isabella</au><au>Pillai, Shiv</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Viewing Siglecs through the lens of tumor immunology</atitle><jtitle>Immunological reviews</jtitle><addtitle>Immunol Rev</addtitle><date>2017-03</date><risdate>2017</risdate><volume>276</volume><issue>1</issue><spage>178</spage><epage>191</epage><pages>178-191</pages><issn>0105-2896</issn><eissn>1600-065X</eissn><abstract>Summary
Many Siglecs function as inhibitory receptors on innate and adaptive immune cells and may contribute to the attenuation of immune responses to tumors. Siglec 9 on neutrophils and Siglec 7 on NK cells are prominent examples of inhibitory Siglecs that can potentially dampen anti‐tumor immunity. CD169 is a Siglec that may function as an adhesion molecule and a facilitator of the recognition and internalization of sialic acid decorated apoptotic bodies and exosomes derived from tumors. It can potentially contribute to both the attenuation as well as the facilitation of anti‐tumor immunity. Siglecs have been best studied in the tumor context in animal models of cancer. Modulators of Siglec function are likely to be developed and investigated clinically in a cancer context over the next few years.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>28258691</pmid><doi>10.1111/imr.12526</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adaptive Immunity Animal models Animals Antigens, CD - immunology Antigens, CD - metabolism Antigens, Differentiation, Myelomonocytic - immunology Antigens, Differentiation, Myelomonocytic - metabolism Apoptosis Attenuation Cancer cancer/tumor immunology Exosomes Humans hypersialylation immune evasion immune regulation Immune response Immune system Immunity Immunity, Innate Immunology Immunomodulation Immunotherapy - methods inhibitory receptor Internalization Killer Cells, Natural - immunology Lectins - immunology Lectins - metabolism Lenses Leukocytes (neutrophilic) Modulators Neoplasms - immunology Neoplasms - therapy Neutrophils - immunology Receptor mechanisms Receptors sialic acid Sialic Acid Binding Ig-like Lectin 1 - immunology Sialic Acid Binding Ig-like Lectin 1 - metabolism Sialic Acid Binding Immunoglobulin-like Lectins - immunology Sialic Acid Binding Immunoglobulin-like Lectins - metabolism Siglec Tumor Escape Tumors |
| title | Viewing Siglecs through the lens of tumor immunology |
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