Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells
Lectin-like transcript-1 (LLT1) (also named osteoclast inhibitory lectin or CLEC2D) is a ligand for the human NKR-P1A (CD161) receptor, present on NK cells and T cells. To further understand the physiological relevance of this interaction, we developed mAbs against LLT1, characterized the expression...
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Veröffentlicht in: | The Journal of immunology (1950) 2008-05, Vol.180 (10), p.6508-6517 |
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creator | Rosen, David B Cao, Wei Avery, Danielle T Tangye, Stuart G Liu, Yong-Jun Houchins, J. P Lanier, Lewis L |
description | Lectin-like transcript-1 (LLT1) (also named osteoclast inhibitory lectin or CLEC2D) is a ligand for the human NKR-P1A (CD161) receptor, present on NK cells and T cells. To further understand the physiological relevance of this interaction, we developed mAbs against LLT1, characterized the expression pattern of LLT1, and explored the functional consequence of LLT1 engagement of the NKR-P1A receptor on NK cells and T cells. LLT1 is expressed on TLR-activated plasmacytoid dendritic, TLR-activated monocyte-derived dendritic cells, and on B cells stimulated through TLR9, surface Ig, or CD40. Interactions between NKR-P1A on NK cells and LLT1 on target cells inhibit NK cell-mediated cytotoxicity and cytokine production and can inhibit TNF-alpha production by TCR-activated NKR-P1A(+) CD8(+) T cells. In contrast, NKR-P1A failed to inhibit or augment the TCR-dependent activation of NKR-P1A-bearing CD4(+) T cells. Expression of LLT1 on activated dendritic cells and B cells suggests that it might regulate the cross-talk between NK cells and APCs. |
doi_str_mv | 10.4049/jimmunol.180.10.6508 |
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In contrast, NKR-P1A failed to inhibit or augment the TCR-dependent activation of NKR-P1A-bearing CD4(+) T cells. Expression of LLT1 on activated dendritic cells and B cells suggests that it might regulate the cross-talk between NK cells and APCs.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.180.10.6508</identifier><identifier>PMID: 18453569</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Antigens, Surface - metabolism ; B-Lymphocytes - metabolism ; Blotting, Western ; Cells, Cultured ; Cytotoxicity, Immunologic - physiology ; Dendritic Cells - metabolism ; Flow Cytometry ; Fluorescent Antibody Technique ; Gene Expression ; Humans ; Immunologic Memory - physiology ; Killer Cells, Natural - metabolism ; Lectins, C-Type - metabolism ; Ligands ; Lymphocyte Activation - immunology ; NK Cell Lectin-Like Receptor Subfamily B ; Oligonucleotide Array Sequence Analysis ; Receptor Cross-Talk - immunology ; Receptors, Cell Surface - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; T-Lymphocytes - metabolism ; Toll-Like Receptors - metabolism</subject><ispartof>The Journal of immunology (1950), 2008-05, Vol.180 (10), p.6508-6517</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c587t-d7928566fe3eff3a816d2b2e687e3699f7a921e395c0533f433b1d16af0eed6b3</citedby><cites>FETCH-LOGICAL-c587t-d7928566fe3eff3a816d2b2e687e3699f7a921e395c0533f433b1d16af0eed6b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18453569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rosen, David B</creatorcontrib><creatorcontrib>Cao, Wei</creatorcontrib><creatorcontrib>Avery, Danielle T</creatorcontrib><creatorcontrib>Tangye, Stuart G</creatorcontrib><creatorcontrib>Liu, Yong-Jun</creatorcontrib><creatorcontrib>Houchins, J. P</creatorcontrib><creatorcontrib>Lanier, Lewis L</creatorcontrib><title>Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Lectin-like transcript-1 (LLT1) (also named osteoclast inhibitory lectin or CLEC2D) is a ligand for the human NKR-P1A (CD161) receptor, present on NK cells and T cells. To further understand the physiological relevance of this interaction, we developed mAbs against LLT1, characterized the expression pattern of LLT1, and explored the functional consequence of LLT1 engagement of the NKR-P1A receptor on NK cells and T cells. LLT1 is expressed on TLR-activated plasmacytoid dendritic, TLR-activated monocyte-derived dendritic cells, and on B cells stimulated through TLR9, surface Ig, or CD40. Interactions between NKR-P1A on NK cells and LLT1 on target cells inhibit NK cell-mediated cytotoxicity and cytokine production and can inhibit TNF-alpha production by TCR-activated NKR-P1A(+) CD8(+) T cells. In contrast, NKR-P1A failed to inhibit or augment the TCR-dependent activation of NKR-P1A-bearing CD4(+) T cells. Expression of LLT1 on activated dendritic cells and B cells suggests that it might regulate the cross-talk between NK cells and APCs.</description><subject>Antigens, Surface - metabolism</subject><subject>B-Lymphocytes - metabolism</subject><subject>Blotting, Western</subject><subject>Cells, Cultured</subject><subject>Cytotoxicity, Immunologic - physiology</subject><subject>Dendritic Cells - metabolism</subject><subject>Flow Cytometry</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene Expression</subject><subject>Humans</subject><subject>Immunologic Memory - physiology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Lectins, C-Type - metabolism</subject><subject>Ligands</subject><subject>Lymphocyte Activation - immunology</subject><subject>NK Cell Lectin-Like Receptor Subfamily B</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Receptor Cross-Talk - immunology</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>T-Lymphocytes - metabolism</subject><subject>Toll-Like Receptors - metabolism</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUGP0zAQhS0EYsvCP0DIJ8QlxY5jJ74glbLLVkSA0HK2nGTSepXYxXY2cOeH424LLCdOHs9878njh9BzSpYFKeTrGzOOk3XDklZkmZqCk-oBWlDOSSYEEQ_RgpA8z2gpyjP0JIQbQoggefEYndGq4IwLuUA_LyfbRuOsHvDa2QDfJrAtBOx6vLERvL6bBtxAnAEsvppGbfHHD1-yz3SFte3wJgZcm-2hrOtrii--7z2EAB12Fq-S_FbHdHkHtvMmmhavYRjCnfTtsX6KHvV6CPDsdJ6jr5cX1-urrP70frNe1VnLqzJmXSnzigvRA4O-Z7qiosubHERVAhNS9qWWOQUmeUs4Y33BWEM7KnRPADrRsHP05ui7n5oRuhZs9HpQe29G7X8op436d2LNTm3drcp5WVJOksHLk4F36aNCVKMJbVpBW3BTUELSkhEp_wvmRAgmKU1gcQRb70Lw0P95DSXqkLP6nbNKOR-ah5yT7MX9Tf6KTsEm4NUR2JntbjYeVBj1MCScqnme73v9Asx4tWw</recordid><startdate>20080515</startdate><enddate>20080515</enddate><creator>Rosen, David B</creator><creator>Cao, Wei</creator><creator>Avery, Danielle T</creator><creator>Tangye, Stuart G</creator><creator>Liu, Yong-Jun</creator><creator>Houchins, J. 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P</au><au>Lanier, Lewis L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2008-05-15</date><risdate>2008</risdate><volume>180</volume><issue>10</issue><spage>6508</spage><epage>6517</epage><pages>6508-6517</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Lectin-like transcript-1 (LLT1) (also named osteoclast inhibitory lectin or CLEC2D) is a ligand for the human NKR-P1A (CD161) receptor, present on NK cells and T cells. To further understand the physiological relevance of this interaction, we developed mAbs against LLT1, characterized the expression pattern of LLT1, and explored the functional consequence of LLT1 engagement of the NKR-P1A receptor on NK cells and T cells. LLT1 is expressed on TLR-activated plasmacytoid dendritic, TLR-activated monocyte-derived dendritic cells, and on B cells stimulated through TLR9, surface Ig, or CD40. Interactions between NKR-P1A on NK cells and LLT1 on target cells inhibit NK cell-mediated cytotoxicity and cytokine production and can inhibit TNF-alpha production by TCR-activated NKR-P1A(+) CD8(+) T cells. In contrast, NKR-P1A failed to inhibit or augment the TCR-dependent activation of NKR-P1A-bearing CD4(+) T cells. Expression of LLT1 on activated dendritic cells and B cells suggests that it might regulate the cross-talk between NK cells and APCs.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>18453569</pmid><doi>10.4049/jimmunol.180.10.6508</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antigens, Surface - metabolism B-Lymphocytes - metabolism Blotting, Western Cells, Cultured Cytotoxicity, Immunologic - physiology Dendritic Cells - metabolism Flow Cytometry Fluorescent Antibody Technique Gene Expression Humans Immunologic Memory - physiology Killer Cells, Natural - metabolism Lectins, C-Type - metabolism Ligands Lymphocyte Activation - immunology NK Cell Lectin-Like Receptor Subfamily B Oligonucleotide Array Sequence Analysis Receptor Cross-Talk - immunology Receptors, Cell Surface - metabolism Reverse Transcriptase Polymerase Chain Reaction T-Lymphocytes - metabolism Toll-Like Receptors - metabolism |
title | Functional Consequences of Interactions between Human NKR-P1A and Its Ligand LLT1 Expressed on Activated Dendritic Cells and B Cells |
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