T Cell Hyporesponsiveness Induced by Oral Administration of Ovalbumin Is Associated with Impaired NFAT Nuclear Translocation and p27kip1 Degradation
Oral tolerance is an important physiological component of the immune system whereby the organism avoids dangerous reactions such as hypersensitivity to ingested food proteins and other luminal Ags which may cause tissue damage and inflammation. In addition, it has been shown in animal models and in...
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| Veröffentlicht in: | The Journal of immunology (1950) 2002-11, Vol.169 (9), p.4723-4731 |
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| container_title | The Journal of immunology (1950) |
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| creator | Asai, Kazumi Hachimura, Satoshi Kimura, Motoko Toraya, Terumasa Yamashita, Masakatsu Nakayama, Toshinori Kaminogawa, Shuichi |
| description | Oral tolerance is an important physiological component of the immune system whereby the organism avoids dangerous reactions such as hypersensitivity to ingested food proteins and other luminal Ags which may cause tissue damage and inflammation. In addition, it has been shown in animal models and in humans that oral tolerance can be applied to controlling undesired immune responses, including autoimmune diseases, allergies, and organ transplant rejections. However, the molecular mechanisms of oral tolerance have been poorly defined. In this study, we investigated the molecular basis underlying the hyporesponsiveness of orally tolerant CD4 T cells using a TCR transgenic mouse system in which oral tolerance was induced by long-term feeding with high dose Ag. We demonstrate that the hyporesponsive state of the CD4 T cells was maintained by a selective impairment in the TCR-induced calcium/NFAT signaling pathway and in the IL-2R-induced degradation of p27(kip1) and cell cycle progression. Thus, physiological mucosal tolerance is revealed to be associated with a unique type of T cell hyporesponsiveness which differs from previously described anergic T cells. |
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In addition, it has been shown in animal models and in humans that oral tolerance can be applied to controlling undesired immune responses, including autoimmune diseases, allergies, and organ transplant rejections. However, the molecular mechanisms of oral tolerance have been poorly defined. In this study, we investigated the molecular basis underlying the hyporesponsiveness of orally tolerant CD4 T cells using a TCR transgenic mouse system in which oral tolerance was induced by long-term feeding with high dose Ag. We demonstrate that the hyporesponsive state of the CD4 T cells was maintained by a selective impairment in the TCR-induced calcium/NFAT signaling pathway and in the IL-2R-induced degradation of p27(kip1) and cell cycle progression. Thus, physiological mucosal tolerance is revealed to be associated with a unique type of T cell hyporesponsiveness which differs from previously described anergic T cells.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>PMID: 12391180</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject><![CDATA[Active Transport, Cell Nucleus - drug effects ; Active Transport, Cell Nucleus - genetics ; Active Transport, Cell Nucleus - immunology ; Adaptor Proteins, Signal Transducing ; Administration, Oral ; Amino Acid Sequence ; Animals ; Antibody Formation - genetics ; Calcium Signaling - drug effects ; Calcium Signaling - genetics ; Calcium Signaling - immunology ; Carrier Proteins - metabolism ; CD4-Positive T-Lymphocytes - drug effects ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; Cell Cycle - genetics ; Cell Cycle - immunology ; Cell Cycle Proteins - metabolism ; Clonal Anergy - drug effects ; Clonal Anergy - genetics ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclin-Dependent Kinases - antagonists & inhibitors ; DNA-Binding Proteins - antagonists & inhibitors ; DNA-Binding Proteins - metabolism ; Dose-Response Relationship, Immunologic ; Immediate-Early Proteins - biosynthesis ; Interleukin-2 - pharmacology ; Ionomycin - pharmacology ; Isoenzymes - antagonists & inhibitors ; Isoenzymes - metabolism ; MAP Kinase Kinase 4 ; MAP Kinase Signaling System - genetics ; MAP Kinase Signaling System - immunology ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Mice, Transgenic ; Milk Proteins ; Mitogen-Activated Protein Kinase Kinases - physiology ; Mitogen-Activated Protein Kinases - physiology ; Molecular Sequence Data ; NFATC Transcription Factors ; Nuclear Proteins ; Ovalbumin - administration & dosage ; Ovalbumin - immunology ; Phospholipase C gamma ; Phosphoproteins - metabolism ; Phosphorylation ; Protein-Tyrosine Kinases - metabolism ; Receptors, Antigen, T-Cell - metabolism ; Receptors, Antigen, T-Cell, alpha-beta - genetics ; Receptors, Interleukin-2 - biosynthesis ; Spleen - cytology ; Spleen - immunology ; Spleen - metabolism ; STAT5 Transcription Factor ; Suppressor of Cytokine Signaling Proteins ; Trans-Activators - metabolism ; Transcription Factors - antagonists & inhibitors ; Transcription Factors - metabolism ; Tumor Suppressor Proteins - metabolism ; Type C Phospholipases - antagonists & inhibitors ; Type C Phospholipases - metabolism ; Tyrosine - metabolism ; ZAP-70 Protein-Tyrosine Kinase]]></subject><ispartof>The Journal of immunology (1950), 2002-11, Vol.169 (9), p.4723-4731</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12391180$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Asai, Kazumi</creatorcontrib><creatorcontrib>Hachimura, Satoshi</creatorcontrib><creatorcontrib>Kimura, Motoko</creatorcontrib><creatorcontrib>Toraya, Terumasa</creatorcontrib><creatorcontrib>Yamashita, Masakatsu</creatorcontrib><creatorcontrib>Nakayama, Toshinori</creatorcontrib><creatorcontrib>Kaminogawa, Shuichi</creatorcontrib><title>T Cell Hyporesponsiveness Induced by Oral Administration of Ovalbumin Is Associated with Impaired NFAT Nuclear Translocation and p27kip1 Degradation</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Oral tolerance is an important physiological component of the immune system whereby the organism avoids dangerous reactions such as hypersensitivity to ingested food proteins and other luminal Ags which may cause tissue damage and inflammation. In addition, it has been shown in animal models and in humans that oral tolerance can be applied to controlling undesired immune responses, including autoimmune diseases, allergies, and organ transplant rejections. However, the molecular mechanisms of oral tolerance have been poorly defined. In this study, we investigated the molecular basis underlying the hyporesponsiveness of orally tolerant CD4 T cells using a TCR transgenic mouse system in which oral tolerance was induced by long-term feeding with high dose Ag. We demonstrate that the hyporesponsive state of the CD4 T cells was maintained by a selective impairment in the TCR-induced calcium/NFAT signaling pathway and in the IL-2R-induced degradation of p27(kip1) and cell cycle progression. Thus, physiological mucosal tolerance is revealed to be associated with a unique type of T cell hyporesponsiveness which differs from previously described anergic T cells.</description><subject>Active Transport, Cell Nucleus - drug effects</subject><subject>Active Transport, Cell Nucleus - genetics</subject><subject>Active Transport, Cell Nucleus - immunology</subject><subject>Adaptor Proteins, Signal Transducing</subject><subject>Administration, Oral</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Antibody Formation - genetics</subject><subject>Calcium Signaling - drug effects</subject><subject>Calcium Signaling - genetics</subject><subject>Calcium Signaling - immunology</subject><subject>Carrier Proteins - metabolism</subject><subject>CD4-Positive T-Lymphocytes - drug effects</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Cell Cycle - genetics</subject><subject>Cell Cycle - immunology</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Clonal Anergy - drug effects</subject><subject>Clonal Anergy - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p27</subject><subject>Cyclin-Dependent Kinases - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - antagonists & inhibitors</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Dose-Response Relationship, Immunologic</subject><subject>Immediate-Early Proteins - biosynthesis</subject><subject>Interleukin-2 - pharmacology</subject><subject>Ionomycin - pharmacology</subject><subject>Isoenzymes - antagonists & inhibitors</subject><subject>Isoenzymes - metabolism</subject><subject>MAP Kinase Kinase 4</subject><subject>MAP Kinase Signaling System - genetics</subject><subject>MAP Kinase Signaling System - immunology</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Milk Proteins</subject><subject>Mitogen-Activated Protein Kinase Kinases - physiology</subject><subject>Mitogen-Activated Protein Kinases - physiology</subject><subject>Molecular Sequence Data</subject><subject>NFATC Transcription Factors</subject><subject>Nuclear Proteins</subject><subject>Ovalbumin - administration & dosage</subject><subject>Ovalbumin - immunology</subject><subject>Phospholipase C gamma</subject><subject>Phosphoproteins - metabolism</subject><subject>Phosphorylation</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>Receptors, Antigen, T-Cell - metabolism</subject><subject>Receptors, Antigen, T-Cell, alpha-beta - genetics</subject><subject>Receptors, Interleukin-2 - biosynthesis</subject><subject>Spleen - cytology</subject><subject>Spleen - immunology</subject><subject>Spleen - metabolism</subject><subject>STAT5 Transcription Factor</subject><subject>Suppressor of Cytokine Signaling Proteins</subject><subject>Trans-Activators - metabolism</subject><subject>Transcription Factors - antagonists & inhibitors</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Type C Phospholipases - antagonists & inhibitors</subject><subject>Type C Phospholipases - metabolism</subject><subject>Tyrosine - metabolism</subject><subject>ZAP-70 Protein-Tyrosine Kinase</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtu2zAQRYWgReOm_YWAq3QlYIaSSGppuElsIIg37loYilTMhHqUlCL4P_rBEeJk3dVgLs69i3ORrLAoIBUCxJdkBcB5ilLIy-R7jM8AIIDn35JL5FmJqGCV_DuwjfWebU9DH2wc-i66V9vZGNmuM1NtDdMntg_k2dq0rnNxDDS6vmN9w_av5PW0pGwX2TrGvnY0Lo3ZjUe2awdyYfke79YH9jjV3lJgh0Bd9H193qDOsIHLFzcg-22fApn3_EfytSEf7c-Pe5X8ubs9bLbpw_5-t1k_pEdECSkWdYkaVdY0ecNBcV0KwoIArG4wzwUqpUEoUyhJoEhLNI3Oi9IaLqyk7Cq5Oe8Oof872ThWrYv1ooM620-xkrxAVXL5XxBVAQIhX8DrD3DSrTXVEFxL4VR9Cl-AX2fg6J6O8-Knii15v-BYzfOMoqzKKpc8y94AMwaLww</recordid><startdate>20021101</startdate><enddate>20021101</enddate><creator>Asai, Kazumi</creator><creator>Hachimura, Satoshi</creator><creator>Kimura, Motoko</creator><creator>Toraya, Terumasa</creator><creator>Yamashita, Masakatsu</creator><creator>Nakayama, Toshinori</creator><creator>Kaminogawa, Shuichi</creator><general>Am Assoc Immnol</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20021101</creationdate><title>T Cell Hyporesponsiveness Induced by Oral Administration of Ovalbumin Is Associated with Impaired NFAT Nuclear Translocation and p27kip1 Degradation</title><author>Asai, Kazumi ; Hachimura, Satoshi ; Kimura, Motoko ; Toraya, Terumasa ; Yamashita, Masakatsu ; Nakayama, Toshinori ; Kaminogawa, Shuichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h1170-15c91b183ff4f2082b96a15a00ebf1446188b068d587a08ab71dfb459ed26e7a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Active Transport, Cell Nucleus - drug effects</topic><topic>Active Transport, Cell Nucleus - genetics</topic><topic>Active Transport, Cell Nucleus - immunology</topic><topic>Adaptor Proteins, Signal Transducing</topic><topic>Administration, Oral</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Antibody Formation - genetics</topic><topic>Calcium Signaling - drug effects</topic><topic>Calcium Signaling - genetics</topic><topic>Calcium Signaling - immunology</topic><topic>Carrier Proteins - metabolism</topic><topic>CD4-Positive T-Lymphocytes - drug effects</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Cell Cycle - genetics</topic><topic>Cell Cycle - immunology</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Clonal Anergy - drug effects</topic><topic>Clonal Anergy - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p27</topic><topic>Cyclin-Dependent Kinases - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - antagonists & inhibitors</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Dose-Response Relationship, Immunologic</topic><topic>Immediate-Early Proteins - biosynthesis</topic><topic>Interleukin-2 - pharmacology</topic><topic>Ionomycin - pharmacology</topic><topic>Isoenzymes - antagonists & inhibitors</topic><topic>Isoenzymes - metabolism</topic><topic>MAP Kinase Kinase 4</topic><topic>MAP Kinase Signaling System - genetics</topic><topic>MAP Kinase Signaling System - immunology</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Milk Proteins</topic><topic>Mitogen-Activated Protein Kinase Kinases - physiology</topic><topic>Mitogen-Activated Protein Kinases - physiology</topic><topic>Molecular Sequence Data</topic><topic>NFATC Transcription Factors</topic><topic>Nuclear Proteins</topic><topic>Ovalbumin - administration & dosage</topic><topic>Ovalbumin - immunology</topic><topic>Phospholipase C gamma</topic><topic>Phosphoproteins - metabolism</topic><topic>Phosphorylation</topic><topic>Protein-Tyrosine Kinases - metabolism</topic><topic>Receptors, Antigen, T-Cell - metabolism</topic><topic>Receptors, Antigen, T-Cell, alpha-beta - genetics</topic><topic>Receptors, Interleukin-2 - biosynthesis</topic><topic>Spleen - cytology</topic><topic>Spleen - immunology</topic><topic>Spleen - metabolism</topic><topic>STAT5 Transcription Factor</topic><topic>Suppressor of Cytokine Signaling Proteins</topic><topic>Trans-Activators - metabolism</topic><topic>Transcription Factors - antagonists & inhibitors</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>Type C Phospholipases - antagonists & inhibitors</topic><topic>Type C Phospholipases - metabolism</topic><topic>Tyrosine - metabolism</topic><topic>ZAP-70 Protein-Tyrosine Kinase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asai, Kazumi</creatorcontrib><creatorcontrib>Hachimura, Satoshi</creatorcontrib><creatorcontrib>Kimura, Motoko</creatorcontrib><creatorcontrib>Toraya, Terumasa</creatorcontrib><creatorcontrib>Yamashita, Masakatsu</creatorcontrib><creatorcontrib>Nakayama, Toshinori</creatorcontrib><creatorcontrib>Kaminogawa, Shuichi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Asai, Kazumi</au><au>Hachimura, Satoshi</au><au>Kimura, Motoko</au><au>Toraya, Terumasa</au><au>Yamashita, Masakatsu</au><au>Nakayama, Toshinori</au><au>Kaminogawa, Shuichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>T Cell Hyporesponsiveness Induced by Oral Administration of Ovalbumin Is Associated with Impaired NFAT Nuclear Translocation and p27kip1 Degradation</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2002-11-01</date><risdate>2002</risdate><volume>169</volume><issue>9</issue><spage>4723</spage><epage>4731</epage><pages>4723-4731</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Oral tolerance is an important physiological component of the immune system whereby the organism avoids dangerous reactions such as hypersensitivity to ingested food proteins and other luminal Ags which may cause tissue damage and inflammation. In addition, it has been shown in animal models and in humans that oral tolerance can be applied to controlling undesired immune responses, including autoimmune diseases, allergies, and organ transplant rejections. However, the molecular mechanisms of oral tolerance have been poorly defined. In this study, we investigated the molecular basis underlying the hyporesponsiveness of orally tolerant CD4 T cells using a TCR transgenic mouse system in which oral tolerance was induced by long-term feeding with high dose Ag. We demonstrate that the hyporesponsive state of the CD4 T cells was maintained by a selective impairment in the TCR-induced calcium/NFAT signaling pathway and in the IL-2R-induced degradation of p27(kip1) and cell cycle progression. Thus, physiological mucosal tolerance is revealed to be associated with a unique type of T cell hyporesponsiveness which differs from previously described anergic T cells.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>12391180</pmid><tpages>9</tpages></addata></record> |
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| ispartof | The Journal of immunology (1950), 2002-11, Vol.169 (9), p.4723-4731 |
| issn | 0022-1767 1550-6606 |
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| subjects | Active Transport, Cell Nucleus - drug effects Active Transport, Cell Nucleus - genetics Active Transport, Cell Nucleus - immunology Adaptor Proteins, Signal Transducing Administration, Oral Amino Acid Sequence Animals Antibody Formation - genetics Calcium Signaling - drug effects Calcium Signaling - genetics Calcium Signaling - immunology Carrier Proteins - metabolism CD4-Positive T-Lymphocytes - drug effects CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism Cell Cycle - genetics Cell Cycle - immunology Cell Cycle Proteins - metabolism Clonal Anergy - drug effects Clonal Anergy - genetics Cyclin-Dependent Kinase Inhibitor p27 Cyclin-Dependent Kinases - antagonists & inhibitors DNA-Binding Proteins - antagonists & inhibitors DNA-Binding Proteins - metabolism Dose-Response Relationship, Immunologic Immediate-Early Proteins - biosynthesis Interleukin-2 - pharmacology Ionomycin - pharmacology Isoenzymes - antagonists & inhibitors Isoenzymes - metabolism MAP Kinase Kinase 4 MAP Kinase Signaling System - genetics MAP Kinase Signaling System - immunology Membrane Proteins - metabolism Mice Mice, Inbred BALB C Mice, Knockout Mice, Transgenic Milk Proteins Mitogen-Activated Protein Kinase Kinases - physiology Mitogen-Activated Protein Kinases - physiology Molecular Sequence Data NFATC Transcription Factors Nuclear Proteins Ovalbumin - administration & dosage Ovalbumin - immunology Phospholipase C gamma Phosphoproteins - metabolism Phosphorylation Protein-Tyrosine Kinases - metabolism Receptors, Antigen, T-Cell - metabolism Receptors, Antigen, T-Cell, alpha-beta - genetics Receptors, Interleukin-2 - biosynthesis Spleen - cytology Spleen - immunology Spleen - metabolism STAT5 Transcription Factor Suppressor of Cytokine Signaling Proteins Trans-Activators - metabolism Transcription Factors - antagonists & inhibitors Transcription Factors - metabolism Tumor Suppressor Proteins - metabolism Type C Phospholipases - antagonists & inhibitors Type C Phospholipases - metabolism Tyrosine - metabolism ZAP-70 Protein-Tyrosine Kinase |
| title | T Cell Hyporesponsiveness Induced by Oral Administration of Ovalbumin Is Associated with Impaired NFAT Nuclear Translocation and p27kip1 Degradation |
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