Misregulation of suppressors of cytokine signaling in eosinophilic esophagitis
Background Several findings suggest that eosinophilic esophagitis (EoE) is strongly associated with atopy and allergen-driven, Th2-type immune responses, indicating the association of EoE with immune dysregulation. The objective of this study is to ascertain the molecular mechanism involved in EoE d...
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| Veröffentlicht in: | Journal of gastroenterology 2013-08, Vol.48 (8), p.910-920 |
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| creator | Zafra, Mª Paz Cancelliere, Natally Rodríguez del Río, Pablo Ruiz-García, Mónica Estévez, Laura Andregnette, Victoria Sánchez-García, Silvia Fiandor, Ana Collantes, Elena Sastre, Joaquín Quirce, Santiago Ibáñez, María Dolores del Pozo, Victoria |
| description | Background
Several findings suggest that eosinophilic esophagitis (EoE) is strongly associated with atopy and allergen-driven, Th2-type immune responses, indicating the association of EoE with immune dysregulation. The objective of this study is to ascertain the molecular mechanism involved in EoE disease development a Th2 condition.
Methods
25 patients with diagnosis of EoE and 17 non-EoE controls were recruited by the gastroenterology and allergy departments from three different hospitals. Transcription analysis of suppressors of cytokine signaling 1, 3, 5 (SOCS), interleukin-5 (IL), IL-13, eotaxin (CCL26), eoataxin receptor (CCR3), and mitogen-activated protein kinase 1 (MAPK1) was performed in esophageal biopsies by real time PCR. Western blot of ERK esophageal protein and additional measures of IL-5 and VEGF levels in serum were performed.
Results
The esophagus of EoE patients expresses and synthesizes high levels of SOCS1 and SOCS3 proteins (
P
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| doi_str_mv | 10.1007/s00535-012-0723-8 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1464508858</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A714585594</galeid><sourcerecordid>A714585594</sourcerecordid><originalsourceid>FETCH-LOGICAL-c591t-6a8fde6379a5944c577a7dd0a10bff7a5628e39de13e31194d10ff6561199e673</originalsourceid><addsrcrecordid>eNqNkUtv1TAQhS0EopfCD2CDIrFhkzJ-xfayqnhJLd2UteUm4-CSawc7WfTf43DLU1RCXng8_s5ojg4hzymcUAD1ugBILlugrAXFeKsfkB0VtSMNYw_JDowQLaVKHJEnpdwAUA5SPyZHjDNmlIId-XgRSsZxndwSUmySb8o6zxlLSblsz_52SV9CxKaEMbopxLEJscFUQkzz5zCFvsFSKzeGJZSn5JF3U8Fnd_cx-fT2zdXZ-_b88t2Hs9PztpeGLm3ntB-w48o4WXfspVJODQM4CtfeKyc7ppGbASlHTqkRAwXvO9nV2mCn-DF5dZg75_R1xbLYfSg9TpOLmNZiqeiEBK2l_g-UdQBaAFT05V_oTVpzdf2d4kxyo-gvanQT2hB9WrLrt6H2VFEhtayeKnXyD6qeAfehTxF9qP0_BPQg6HMqNRNv5xz2Lt9aCnaL2x7itjVuu8VtN28v7hZer_c4_FT8yLcC7ACU-hVHzL85unfqN7ZGsrE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1423253971</pqid></control><display><type>article</type><title>Misregulation of suppressors of cytokine signaling in eosinophilic esophagitis</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Zafra, Mª Paz ; Cancelliere, Natally ; Rodríguez del Río, Pablo ; Ruiz-García, Mónica ; Estévez, Laura ; Andregnette, Victoria ; Sánchez-García, Silvia ; Fiandor, Ana ; Collantes, Elena ; Sastre, Joaquín ; Quirce, Santiago ; Ibáñez, María Dolores ; del Pozo, Victoria</creator><creatorcontrib>Zafra, Mª Paz ; Cancelliere, Natally ; Rodríguez del Río, Pablo ; Ruiz-García, Mónica ; Estévez, Laura ; Andregnette, Victoria ; Sánchez-García, Silvia ; Fiandor, Ana ; Collantes, Elena ; Sastre, Joaquín ; Quirce, Santiago ; Ibáñez, María Dolores ; del Pozo, Victoria</creatorcontrib><description>Background
Several findings suggest that eosinophilic esophagitis (EoE) is strongly associated with atopy and allergen-driven, Th2-type immune responses, indicating the association of EoE with immune dysregulation. The objective of this study is to ascertain the molecular mechanism involved in EoE disease development a Th2 condition.
Methods
25 patients with diagnosis of EoE and 17 non-EoE controls were recruited by the gastroenterology and allergy departments from three different hospitals. Transcription analysis of suppressors of cytokine signaling 1, 3, 5 (SOCS), interleukin-5 (IL), IL-13, eotaxin (CCL26), eoataxin receptor (CCR3), and mitogen-activated protein kinase 1 (MAPK1) was performed in esophageal biopsies by real time PCR. Western blot of ERK esophageal protein and additional measures of IL-5 and VEGF levels in serum were performed.
Results
The esophagus of EoE patients expresses and synthesizes high levels of SOCS1 and SOCS3 proteins (
P
< 0.05), and these expression correlated with levels of IL-5, IL-13, CCL26, CCR3, and MAPK1 genes. In addition, we demonstrate the implication of the ERK pathway (
P
< 0.001).
Conclusions
SOCS proteins probably contribute to EoE pathogenesis by directly or indirectly inducing the Th2 profile, as well as by promoting the production of Th2 cytokines. All these findings further enhance our understanding of the mechanism of EoE, and accumulating evidence suggests that EoE pathogenesis is likely to be due to misregulation of immunological pathways.</description><identifier>ISSN: 0944-1174</identifier><identifier>EISSN: 1435-5922</identifier><identifier>DOI: 10.1007/s00535-012-0723-8</identifier><identifier>PMID: 23229770</identifier><language>eng</language><publisher>Tokyo: Springer Japan</publisher><subject>Abdominal Surgery ; Adolescent ; Adult ; Aged ; Allergens ; Allergic reaction ; Allergy ; Analysis ; Atopy ; Blotting, Western ; Case-Control Studies ; Child ; Colorectal Surgery ; Cross-Sectional Studies ; Cytokines - immunology ; Cytokines - metabolism ; Development and progression ; Diagnosis ; Eosinophilic Esophagitis - immunology ; Eosinophilic Esophagitis - physiopathology ; Esophagitis ; Female ; Gastroenterology ; Hepatology ; Hospitals ; Humans ; Immune response ; Interleukins ; Male ; MAP Kinase Signaling System ; Medicine ; Medicine & Public Health ; Middle Aged ; Mitogens ; Original Article—Alimentary Tract ; Prospective Studies ; Protein kinases ; Real-Time Polymerase Chain Reaction ; Signal Transduction - immunology ; Suppressor of Cytokine Signaling Proteins - metabolism ; Surgical Oncology ; Th2 Cells - immunology ; Vascular endothelial growth factor ; Young Adult</subject><ispartof>Journal of gastroenterology, 2013-08, Vol.48 (8), p.910-920</ispartof><rights>Springer Japan 2012</rights><rights>COPYRIGHT 2013 Springer</rights><rights>Springer Japan 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c591t-6a8fde6379a5944c577a7dd0a10bff7a5628e39de13e31194d10ff6561199e673</citedby><cites>FETCH-LOGICAL-c591t-6a8fde6379a5944c577a7dd0a10bff7a5628e39de13e31194d10ff6561199e673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00535-012-0723-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00535-012-0723-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23229770$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zafra, Mª Paz</creatorcontrib><creatorcontrib>Cancelliere, Natally</creatorcontrib><creatorcontrib>Rodríguez del Río, Pablo</creatorcontrib><creatorcontrib>Ruiz-García, Mónica</creatorcontrib><creatorcontrib>Estévez, Laura</creatorcontrib><creatorcontrib>Andregnette, Victoria</creatorcontrib><creatorcontrib>Sánchez-García, Silvia</creatorcontrib><creatorcontrib>Fiandor, Ana</creatorcontrib><creatorcontrib>Collantes, Elena</creatorcontrib><creatorcontrib>Sastre, Joaquín</creatorcontrib><creatorcontrib>Quirce, Santiago</creatorcontrib><creatorcontrib>Ibáñez, María Dolores</creatorcontrib><creatorcontrib>del Pozo, Victoria</creatorcontrib><title>Misregulation of suppressors of cytokine signaling in eosinophilic esophagitis</title><title>Journal of gastroenterology</title><addtitle>J Gastroenterol</addtitle><addtitle>J Gastroenterol</addtitle><description>Background
Several findings suggest that eosinophilic esophagitis (EoE) is strongly associated with atopy and allergen-driven, Th2-type immune responses, indicating the association of EoE with immune dysregulation. The objective of this study is to ascertain the molecular mechanism involved in EoE disease development a Th2 condition.
Methods
25 patients with diagnosis of EoE and 17 non-EoE controls were recruited by the gastroenterology and allergy departments from three different hospitals. Transcription analysis of suppressors of cytokine signaling 1, 3, 5 (SOCS), interleukin-5 (IL), IL-13, eotaxin (CCL26), eoataxin receptor (CCR3), and mitogen-activated protein kinase 1 (MAPK1) was performed in esophageal biopsies by real time PCR. Western blot of ERK esophageal protein and additional measures of IL-5 and VEGF levels in serum were performed.
Results
The esophagus of EoE patients expresses and synthesizes high levels of SOCS1 and SOCS3 proteins (
P
< 0.05), and these expression correlated with levels of IL-5, IL-13, CCL26, CCR3, and MAPK1 genes. In addition, we demonstrate the implication of the ERK pathway (
P
< 0.001).
Conclusions
SOCS proteins probably contribute to EoE pathogenesis by directly or indirectly inducing the Th2 profile, as well as by promoting the production of Th2 cytokines. All these findings further enhance our understanding of the mechanism of EoE, and accumulating evidence suggests that EoE pathogenesis is likely to be due to misregulation of immunological pathways.</description><subject>Abdominal Surgery</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Allergens</subject><subject>Allergic reaction</subject><subject>Allergy</subject><subject>Analysis</subject><subject>Atopy</subject><subject>Blotting, Western</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Colorectal Surgery</subject><subject>Cross-Sectional Studies</subject><subject>Cytokines - immunology</subject><subject>Cytokines - metabolism</subject><subject>Development and progression</subject><subject>Diagnosis</subject><subject>Eosinophilic Esophagitis - immunology</subject><subject>Eosinophilic Esophagitis - physiopathology</subject><subject>Esophagitis</subject><subject>Female</subject><subject>Gastroenterology</subject><subject>Hepatology</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immune response</subject><subject>Interleukins</subject><subject>Male</subject><subject>MAP Kinase Signaling System</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mitogens</subject><subject>Original Article—Alimentary Tract</subject><subject>Prospective Studies</subject><subject>Protein kinases</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Signal Transduction - immunology</subject><subject>Suppressor of Cytokine Signaling Proteins - metabolism</subject><subject>Surgical Oncology</subject><subject>Th2 Cells - immunology</subject><subject>Vascular endothelial growth factor</subject><subject>Young Adult</subject><issn>0944-1174</issn><issn>1435-5922</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkUtv1TAQhS0EopfCD2CDIrFhkzJ-xfayqnhJLd2UteUm4-CSawc7WfTf43DLU1RCXng8_s5ojg4hzymcUAD1ugBILlugrAXFeKsfkB0VtSMNYw_JDowQLaVKHJEnpdwAUA5SPyZHjDNmlIId-XgRSsZxndwSUmySb8o6zxlLSblsz_52SV9CxKaEMbopxLEJscFUQkzz5zCFvsFSKzeGJZSn5JF3U8Fnd_cx-fT2zdXZ-_b88t2Hs9PztpeGLm3ntB-w48o4WXfspVJODQM4CtfeKyc7ppGbASlHTqkRAwXvO9nV2mCn-DF5dZg75_R1xbLYfSg9TpOLmNZiqeiEBK2l_g-UdQBaAFT05V_oTVpzdf2d4kxyo-gvanQT2hB9WrLrt6H2VFEhtayeKnXyD6qeAfehTxF9qP0_BPQg6HMqNRNv5xz2Lt9aCnaL2x7itjVuu8VtN28v7hZer_c4_FT8yLcC7ACU-hVHzL85unfqN7ZGsrE</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Zafra, Mª Paz</creator><creator>Cancelliere, Natally</creator><creator>Rodríguez del Río, Pablo</creator><creator>Ruiz-García, Mónica</creator><creator>Estévez, Laura</creator><creator>Andregnette, Victoria</creator><creator>Sánchez-García, Silvia</creator><creator>Fiandor, Ana</creator><creator>Collantes, Elena</creator><creator>Sastre, Joaquín</creator><creator>Quirce, Santiago</creator><creator>Ibáñez, María Dolores</creator><creator>del Pozo, Victoria</creator><general>Springer Japan</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20130801</creationdate><title>Misregulation of suppressors of cytokine signaling in eosinophilic esophagitis</title><author>Zafra, Mª Paz ; Cancelliere, Natally ; Rodríguez del Río, Pablo ; Ruiz-García, Mónica ; Estévez, Laura ; Andregnette, Victoria ; Sánchez-García, Silvia ; Fiandor, Ana ; Collantes, Elena ; Sastre, Joaquín ; Quirce, Santiago ; Ibáñez, María Dolores ; del Pozo, Victoria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c591t-6a8fde6379a5944c577a7dd0a10bff7a5628e39de13e31194d10ff6561199e673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Abdominal Surgery</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Allergens</topic><topic>Allergic reaction</topic><topic>Allergy</topic><topic>Analysis</topic><topic>Atopy</topic><topic>Blotting, Western</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Colorectal Surgery</topic><topic>Cross-Sectional Studies</topic><topic>Cytokines - immunology</topic><topic>Cytokines - metabolism</topic><topic>Development and progression</topic><topic>Diagnosis</topic><topic>Eosinophilic Esophagitis - immunology</topic><topic>Eosinophilic Esophagitis - physiopathology</topic><topic>Esophagitis</topic><topic>Female</topic><topic>Gastroenterology</topic><topic>Hepatology</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immune response</topic><topic>Interleukins</topic><topic>Male</topic><topic>MAP Kinase Signaling System</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mitogens</topic><topic>Original Article—Alimentary Tract</topic><topic>Prospective Studies</topic><topic>Protein kinases</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Signal Transduction - immunology</topic><topic>Suppressor of Cytokine Signaling Proteins - metabolism</topic><topic>Surgical Oncology</topic><topic>Th2 Cells - immunology</topic><topic>Vascular endothelial growth factor</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zafra, Mª Paz</creatorcontrib><creatorcontrib>Cancelliere, Natally</creatorcontrib><creatorcontrib>Rodríguez del Río, Pablo</creatorcontrib><creatorcontrib>Ruiz-García, Mónica</creatorcontrib><creatorcontrib>Estévez, Laura</creatorcontrib><creatorcontrib>Andregnette, Victoria</creatorcontrib><creatorcontrib>Sánchez-García, Silvia</creatorcontrib><creatorcontrib>Fiandor, Ana</creatorcontrib><creatorcontrib>Collantes, Elena</creatorcontrib><creatorcontrib>Sastre, Joaquín</creatorcontrib><creatorcontrib>Quirce, Santiago</creatorcontrib><creatorcontrib>Ibáñez, María Dolores</creatorcontrib><creatorcontrib>del Pozo, Victoria</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Proquest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of gastroenterology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zafra, Mª Paz</au><au>Cancelliere, Natally</au><au>Rodríguez del Río, Pablo</au><au>Ruiz-García, Mónica</au><au>Estévez, Laura</au><au>Andregnette, Victoria</au><au>Sánchez-García, Silvia</au><au>Fiandor, Ana</au><au>Collantes, Elena</au><au>Sastre, Joaquín</au><au>Quirce, Santiago</au><au>Ibáñez, María Dolores</au><au>del Pozo, Victoria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Misregulation of suppressors of cytokine signaling in eosinophilic esophagitis</atitle><jtitle>Journal of gastroenterology</jtitle><stitle>J Gastroenterol</stitle><addtitle>J Gastroenterol</addtitle><date>2013-08-01</date><risdate>2013</risdate><volume>48</volume><issue>8</issue><spage>910</spage><epage>920</epage><pages>910-920</pages><issn>0944-1174</issn><eissn>1435-5922</eissn><abstract>Background
Several findings suggest that eosinophilic esophagitis (EoE) is strongly associated with atopy and allergen-driven, Th2-type immune responses, indicating the association of EoE with immune dysregulation. The objective of this study is to ascertain the molecular mechanism involved in EoE disease development a Th2 condition.
Methods
25 patients with diagnosis of EoE and 17 non-EoE controls were recruited by the gastroenterology and allergy departments from three different hospitals. Transcription analysis of suppressors of cytokine signaling 1, 3, 5 (SOCS), interleukin-5 (IL), IL-13, eotaxin (CCL26), eoataxin receptor (CCR3), and mitogen-activated protein kinase 1 (MAPK1) was performed in esophageal biopsies by real time PCR. Western blot of ERK esophageal protein and additional measures of IL-5 and VEGF levels in serum were performed.
Results
The esophagus of EoE patients expresses and synthesizes high levels of SOCS1 and SOCS3 proteins (
P
< 0.05), and these expression correlated with levels of IL-5, IL-13, CCL26, CCR3, and MAPK1 genes. In addition, we demonstrate the implication of the ERK pathway (
P
< 0.001).
Conclusions
SOCS proteins probably contribute to EoE pathogenesis by directly or indirectly inducing the Th2 profile, as well as by promoting the production of Th2 cytokines. All these findings further enhance our understanding of the mechanism of EoE, and accumulating evidence suggests that EoE pathogenesis is likely to be due to misregulation of immunological pathways.</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>23229770</pmid><doi>10.1007/s00535-012-0723-8</doi><tpages>11</tpages></addata></record> |
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| identifier | ISSN: 0944-1174 |
| ispartof | Journal of gastroenterology, 2013-08, Vol.48 (8), p.910-920 |
| issn | 0944-1174 1435-5922 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Abdominal Surgery Adolescent Adult Aged Allergens Allergic reaction Allergy Analysis Atopy Blotting, Western Case-Control Studies Child Colorectal Surgery Cross-Sectional Studies Cytokines - immunology Cytokines - metabolism Development and progression Diagnosis Eosinophilic Esophagitis - immunology Eosinophilic Esophagitis - physiopathology Esophagitis Female Gastroenterology Hepatology Hospitals Humans Immune response Interleukins Male MAP Kinase Signaling System Medicine Medicine & Public Health Middle Aged Mitogens Original Article—Alimentary Tract Prospective Studies Protein kinases Real-Time Polymerase Chain Reaction Signal Transduction - immunology Suppressor of Cytokine Signaling Proteins - metabolism Surgical Oncology Th2 Cells - immunology Vascular endothelial growth factor Young Adult |
| title | Misregulation of suppressors of cytokine signaling in eosinophilic esophagitis |
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