Granzyme B Is Critical for T Cell Receptor-Induced Cell Death of Type 2 Helper T Cells
Although CD95L is required for T cell receptor (TCR)-induced cell death (TCR-ICD) in T helper 1 cells, the molecular mechanisms mediating TCR-ICD in Th2 cells are unknown. We found that death receptors were not involved in TCR-ICD of Th2 cells because blocking their cognate ligands had no effect on...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2006-08, Vol.25 (2), p.237-247 |
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| creator | Devadas, Satish Das, Jyoti Liu, Catherine Zhang, Liying Roberts, Arthur I. Pan, Zui Moore, Paul A. Das, Gobardhan Shi, Yufang |
| description | Although CD95L is required for T cell receptor (TCR)-induced cell death (TCR-ICD) in T helper 1 cells, the molecular mechanisms mediating TCR-ICD in Th2 cells are unknown. We found that death receptors were not involved in TCR-ICD of Th2 cells because blocking their cognate ligands had no effect on apoptosis of activated Th2 cells. Furthermore, we showed that caspases were not actively involved in TCR-ICD of Th2 cells. However, inhibition of granzyme B (GrB) activity abolished TCR-ICD in Th2 cells but not Th1 cells. Likewise, Th2 cells derived from GrB-deficient mice were resistant to TCR-ICD, and GrB deficiency or inhibition of GrB activity consequently enhanced the production of Th2 cytokines. GrB-deficient mice exhibited increased susceptibility to allergen-induced asthma. Thus, GrB plays a critical role in the TCR-ICD of Th2 cells. |
| doi_str_mv | 10.1016/j.immuni.2006.06.011 |
| format | Article |
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We found that death receptors were not involved in TCR-ICD of Th2 cells because blocking their cognate ligands had no effect on apoptosis of activated Th2 cells. Furthermore, we showed that caspases were not actively involved in TCR-ICD of Th2 cells. However, inhibition of granzyme B (GrB) activity abolished TCR-ICD in Th2 cells but not Th1 cells. Likewise, Th2 cells derived from GrB-deficient mice were resistant to TCR-ICD, and GrB deficiency or inhibition of GrB activity consequently enhanced the production of Th2 cytokines. GrB-deficient mice exhibited increased susceptibility to allergen-induced asthma. Thus, GrB plays a critical role in the TCR-ICD of Th2 cells.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2006.06.011</identifier><identifier>PMID: 16901729</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Allergens - immunology ; Animals ; Apoptosis ; Apoptosis - immunology ; Asthma - immunology ; Asthma - pathology ; Biomedical research ; Caspases - metabolism ; Cell death ; CELLIMMUNO ; Cells, Cultured ; Cytokines ; Cytotoxicity ; Deoxyribonucleic acid ; DNA ; Enzyme Activation ; Female ; Flow cytometry ; Granzymes ; Immune system ; Lymphocytes ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; MOLIMMUNO ; Receptors, Antigen, T-Cell - immunology ; Serine Endopeptidases - deficiency ; Serine Endopeptidases - genetics ; Serine Endopeptidases - metabolism ; Statistical analysis ; T cell receptors ; Th1 Cells - cytology ; Th1 Cells - immunology ; Th1 Cells - metabolism ; Th2 Cells - cytology ; Th2 Cells - immunology ; Th2 Cells - metabolism ; Time Factors ; Tumor Necrosis Factor-alpha - metabolism ; Variance analysis</subject><ispartof>Immunity (Cambridge, Mass.), 2006-08, Vol.25 (2), p.237-247</ispartof><rights>2006 Elsevier Inc.</rights><rights>Copyright Elsevier Limited Aug 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c465t-7942923ec6a5f5f28f13b026fdb5c1978d5d880be61a6b0114c09dbaf1d5d7ed3</citedby><cites>FETCH-LOGICAL-c465t-7942923ec6a5f5f28f13b026fdb5c1978d5d880be61a6b0114c09dbaf1d5d7ed3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.immuni.2006.06.011$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16901729$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Devadas, Satish</creatorcontrib><creatorcontrib>Das, Jyoti</creatorcontrib><creatorcontrib>Liu, Catherine</creatorcontrib><creatorcontrib>Zhang, Liying</creatorcontrib><creatorcontrib>Roberts, Arthur I.</creatorcontrib><creatorcontrib>Pan, Zui</creatorcontrib><creatorcontrib>Moore, Paul A.</creatorcontrib><creatorcontrib>Das, Gobardhan</creatorcontrib><creatorcontrib>Shi, Yufang</creatorcontrib><title>Granzyme B Is Critical for T Cell Receptor-Induced Cell Death of Type 2 Helper T Cells</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>Although CD95L is required for T cell receptor (TCR)-induced cell death (TCR-ICD) in T helper 1 cells, the molecular mechanisms mediating TCR-ICD in Th2 cells are unknown. 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Thus, GrB plays a critical role in the TCR-ICD of Th2 cells.</description><subject>Allergens - immunology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - immunology</subject><subject>Asthma - immunology</subject><subject>Asthma - pathology</subject><subject>Biomedical research</subject><subject>Caspases - metabolism</subject><subject>Cell death</subject><subject>CELLIMMUNO</subject><subject>Cells, Cultured</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>Flow cytometry</subject><subject>Granzymes</subject><subject>Immune system</subject><subject>Lymphocytes</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>MOLIMMUNO</subject><subject>Receptors, Antigen, T-Cell - immunology</subject><subject>Serine Endopeptidases - deficiency</subject><subject>Serine Endopeptidases - genetics</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Statistical analysis</subject><subject>T cell receptors</subject><subject>Th1 Cells - cytology</subject><subject>Th1 Cells - immunology</subject><subject>Th1 Cells - metabolism</subject><subject>Th2 Cells - cytology</subject><subject>Th2 Cells - immunology</subject><subject>Th2 Cells - metabolism</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Variance analysis</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV-L1DAUxYso7rr6DUQCgm8dc9M0aV4EHXV3YEGQ0deQJjeYof9MWmH89KZ0RPBB4UJC8js3uecUxXOgO6AgXp92oe-XIewYpWK3FsCD4hqokiWHhj5c95KXUkB1VTxJ6UQp8FrRx8UVCEVBMnVdfL2NZvh57pG8I4dE9jHMwZqO-DGSI9lj15HPaHGax1geBrdYdNvpezTzNzJ6cjxPSBi5w27C35r0tHjkTZfw2WW9Kb58_HDc35X3n24P-7f3peWinkupOFOsQitM7WvPGg9VS5nwrq0tKNm42jUNbVGAEW0ekFuqXGs85AuJrropXm19pzh-XzDNug_J5h-YAccladFIISRU_wVBVdnUSmTw5V_gaVzikIfQUFPOKsE4zRTfKBvHlCJ6PcXQm3jWQPUajz7pLR69xqPXAsiyF5fmS9uj-yO65JGBNxuA2bQfAaNONuCQXQ8R7azdGP79wi8k_p-o</recordid><startdate>20060801</startdate><enddate>20060801</enddate><creator>Devadas, Satish</creator><creator>Das, Jyoti</creator><creator>Liu, Catherine</creator><creator>Zhang, Liying</creator><creator>Roberts, Arthur I.</creator><creator>Pan, Zui</creator><creator>Moore, Paul A.</creator><creator>Das, Gobardhan</creator><creator>Shi, Yufang</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20060801</creationdate><title>Granzyme B Is Critical for T Cell Receptor-Induced Cell Death of Type 2 Helper T Cells</title><author>Devadas, Satish ; 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We found that death receptors were not involved in TCR-ICD of Th2 cells because blocking their cognate ligands had no effect on apoptosis of activated Th2 cells. Furthermore, we showed that caspases were not actively involved in TCR-ICD of Th2 cells. However, inhibition of granzyme B (GrB) activity abolished TCR-ICD in Th2 cells but not Th1 cells. Likewise, Th2 cells derived from GrB-deficient mice were resistant to TCR-ICD, and GrB deficiency or inhibition of GrB activity consequently enhanced the production of Th2 cytokines. GrB-deficient mice exhibited increased susceptibility to allergen-induced asthma. Thus, GrB plays a critical role in the TCR-ICD of Th2 cells.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16901729</pmid><doi>10.1016/j.immuni.2006.06.011</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Allergens - immunology Animals Apoptosis Apoptosis - immunology Asthma - immunology Asthma - pathology Biomedical research Caspases - metabolism Cell death CELLIMMUNO Cells, Cultured Cytokines Cytotoxicity Deoxyribonucleic acid DNA Enzyme Activation Female Flow cytometry Granzymes Immune system Lymphocytes Mice Mice, Inbred BALB C Mice, Knockout MOLIMMUNO Receptors, Antigen, T-Cell - immunology Serine Endopeptidases - deficiency Serine Endopeptidases - genetics Serine Endopeptidases - metabolism Statistical analysis T cell receptors Th1 Cells - cytology Th1 Cells - immunology Th1 Cells - metabolism Th2 Cells - cytology Th2 Cells - immunology Th2 Cells - metabolism Time Factors Tumor Necrosis Factor-alpha - metabolism Variance analysis |
| title | Granzyme B Is Critical for T Cell Receptor-Induced Cell Death of Type 2 Helper T Cells |
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