MicroRNA-23b promotes tolerogenic properties of dendritic cells in vitro through inhibiting Notch1/NF-κB signalling pathways
Background: MicroRNAs (miRNAs) are known to regulate the inflammatory response in various cell types. However, the ability of miRNAs to modulate dendritic cells (DCs) function for allergen immunotherapy is unclear. Objective: To assess the role of miR‐23b in the regulation of ovalbumin (OVA)‐induced...
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| Veröffentlicht in: | Allergy (Copenhagen) 2012-03, Vol.67 (3), p.362-370 |
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| creator | Zheng, J. Jiang, H.-Y. Li, J. Tang, H.-C. Zhang, X.-M. Wang, X.-R. Du, J.-T. Li, H.-B. Xu, G. |
| description | Background:
MicroRNAs (miRNAs) are known to regulate the inflammatory response in various cell types. However, the ability of miRNAs to modulate dendritic cells (DCs) function for allergen immunotherapy is unclear.
Objective:
To assess the role of miR‐23b in the regulation of ovalbumin (OVA)‐induced DC differentiation and function and to investigate the related molecular mechanisms.
Methods:
Bone marrow‐derived dendritic cells (BMDCs) were generated from murine bone marrow progenitor cells and subsequently stimulated with OVA to examine the profile of miRNA expression. After transfection with miR‐23b reagents, DCs were evaluated for endocytic ability, surface marker expression, cytokine secretion and CD4+ T‐cell differentiation. The possible roles of the Notch and NF‐κB signalling pathways were also evaluated. Human monocyte‐derived dendritic cells (MDDCs) were similarly evaluated as well.
Results:
Significant upregulation of miR‐23b was observed in BMDCs pulsed with OVA. Following miR‐23b transfection, BMDCs showed decreased OVA uptake, increased IL‐10 production, decreased IL‐12 production and an enhanced capacity to promote FoxP3+ CD4+ T regulatory cells (Tregs) differentiation. In addition, inactivation of the Notch1 and NF‐κB signalling pathways were observed. Conversely, inhibition of miR‐23b in BMDCs resulted in the opposite effects. In human MDDCs, miRNA23b transfection similarly increased IL‐10 and decreased IL‐12 production, and that treated human MDDCs induced increased FoxP3+ CD4+ T cells.
Conclusion:
Our findings provide evidence that miR‐23b is capable of inducing tolerogenic DC activity and Treg responses in vitro through the inhibition of the Notch1 and NF‐κB signalling pathways; thus, miR‐23b might represent a therapeutic target for the management of allergic diseases. |
| doi_str_mv | 10.1111/j.1398-9995.2011.02776.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_926887003</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>921426962</sourcerecordid><originalsourceid>FETCH-LOGICAL-i2796-6728f0dde52f27d660d584c21a59ae7d5640e675050286a4b434dc32ed5392f33</originalsourceid><addsrcrecordid>eNqNkc2O0zAUhS0EYsrAK6BsEKtk_BPb8YJFp2JmkEKR0KBKbCw3dhqXNC62y7SLeTEegmfCoaVsuRtb53z36toHgAzBAqW6WheIiCoXQtACQ4QKiDlnxf4JmJyNp2ACEaR5SUl1AV6EsIYQcizgc3CBUwmO2AQ8frSNd5_n0xyTZbb1buOiCVl0vfFuZQbbjOLW-GiT7NpMm0F7G5PemL4PmR2yHzZ6l8XOu92qS0JnlwkYVtncxaZDV_Ob_NfP6yzY1aD6fjS2KnYP6hBegmet6oN5dTovwZeb9_ezu7z-dPthNq1zi7lgOeO4aqHWhuIWc80Y1LQqG4wUFcpwTVkJDeMUUogrpsplSUrdEGw0JQK3hFyCt8e56S3fdyZEubFh3F8Nxu2CFJhVFYfwf0hUYiYYTuTrE7lbboyWW283yh_k379NwJsToEKj-tarobHhH0cZxZDAxL07cg-2N4ezj6Acs5ZrOUYqx0jlmLX8k7Xcy2ldj7fUnx_7bYhmf-5X_ptknHAqF_NbWd8vFvz66ywN-w0bsax6</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>921426962</pqid></control><display><type>article</type><title>MicroRNA-23b promotes tolerogenic properties of dendritic cells in vitro through inhibiting Notch1/NF-κB signalling pathways</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Wiley Free Content</source><creator>Zheng, J. ; Jiang, H.-Y. ; Li, J. ; Tang, H.-C. ; Zhang, X.-M. ; Wang, X.-R. ; Du, J.-T. ; Li, H.-B. ; Xu, G.</creator><creatorcontrib>Zheng, J. ; Jiang, H.-Y. ; Li, J. ; Tang, H.-C. ; Zhang, X.-M. ; Wang, X.-R. ; Du, J.-T. ; Li, H.-B. ; Xu, G.</creatorcontrib><description>Background:
MicroRNAs (miRNAs) are known to regulate the inflammatory response in various cell types. However, the ability of miRNAs to modulate dendritic cells (DCs) function for allergen immunotherapy is unclear.
Objective:
To assess the role of miR‐23b in the regulation of ovalbumin (OVA)‐induced DC differentiation and function and to investigate the related molecular mechanisms.
Methods:
Bone marrow‐derived dendritic cells (BMDCs) were generated from murine bone marrow progenitor cells and subsequently stimulated with OVA to examine the profile of miRNA expression. After transfection with miR‐23b reagents, DCs were evaluated for endocytic ability, surface marker expression, cytokine secretion and CD4+ T‐cell differentiation. The possible roles of the Notch and NF‐κB signalling pathways were also evaluated. Human monocyte‐derived dendritic cells (MDDCs) were similarly evaluated as well.
Results:
Significant upregulation of miR‐23b was observed in BMDCs pulsed with OVA. Following miR‐23b transfection, BMDCs showed decreased OVA uptake, increased IL‐10 production, decreased IL‐12 production and an enhanced capacity to promote FoxP3+ CD4+ T regulatory cells (Tregs) differentiation. In addition, inactivation of the Notch1 and NF‐κB signalling pathways were observed. Conversely, inhibition of miR‐23b in BMDCs resulted in the opposite effects. In human MDDCs, miRNA23b transfection similarly increased IL‐10 and decreased IL‐12 production, and that treated human MDDCs induced increased FoxP3+ CD4+ T cells.
Conclusion:
Our findings provide evidence that miR‐23b is capable of inducing tolerogenic DC activity and Treg responses in vitro through the inhibition of the Notch1 and NF‐κB signalling pathways; thus, miR‐23b might represent a therapeutic target for the management of allergic diseases.</description><identifier>ISSN: 0105-4538</identifier><identifier>EISSN: 1398-9995</identifier><identifier>DOI: 10.1111/j.1398-9995.2011.02776.x</identifier><identifier>PMID: 22229716</identifier><identifier>CODEN: LLRGDY</identifier><language>eng</language><publisher>Oxford: Blackwell Publishing Ltd</publisher><subject>Allergens ; Allergens - administration & dosage ; Allergens - immunology ; Allergic diseases ; Animals ; Biological and medical sciences ; Bone marrow ; Bone Marrow Cells - immunology ; CD4 antigen ; Cell Differentiation ; Cells, Cultured ; Dendritic cells ; Dendritic Cells - cytology ; Dendritic Cells - immunology ; Dendritic Cells - metabolism ; Dermatology ; Differentiation ; Foxp3 protein ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Gene expression ; Humans ; Hypersensitivity - immunology ; Hypersensitivity - therapy ; Immune Tolerance ; Immunoregulation ; Immunotherapy ; in vitro ; Inflammation ; Interleukin 10 ; Interleukin 12 ; Lymphocytes T ; Male ; Medical sciences ; Mice ; Mice, Inbred BALB C ; microRNAs ; MicroRNAs - immunology ; MicroRNAs - metabolism ; MicroRNAs - pharmacology ; miRNA ; Molecular modelling ; Monocytes ; NF- Kappa B protein ; NF-kappa B - antagonists & inhibitors ; NF-κB ; Notch ; Notch protein ; Osteoprogenitor cells ; Ovalbumin ; Ovalbumin - administration & dosage ; Ovalbumin - immunology ; Receptor, Notch1 - antagonists & inhibitors ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Signal transduction ; Signal Transduction - drug effects ; signalling pathway ; Surface markers ; T regulatory cells ; Transfection ; Up-Regulation</subject><ispartof>Allergy (Copenhagen), 2012-03, Vol.67 (3), p.362-370</ispartof><rights>2012 John Wiley & Sons A/S</rights><rights>2015 INIST-CNRS</rights><rights>2012 John Wiley & Sons A/S.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1398-9995.2011.02776.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1398-9995.2011.02776.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,1428,27905,27906,45555,45556,46390,46814</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25652030$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22229716$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zheng, J.</creatorcontrib><creatorcontrib>Jiang, H.-Y.</creatorcontrib><creatorcontrib>Li, J.</creatorcontrib><creatorcontrib>Tang, H.-C.</creatorcontrib><creatorcontrib>Zhang, X.-M.</creatorcontrib><creatorcontrib>Wang, X.-R.</creatorcontrib><creatorcontrib>Du, J.-T.</creatorcontrib><creatorcontrib>Li, H.-B.</creatorcontrib><creatorcontrib>Xu, G.</creatorcontrib><title>MicroRNA-23b promotes tolerogenic properties of dendritic cells in vitro through inhibiting Notch1/NF-κB signalling pathways</title><title>Allergy (Copenhagen)</title><addtitle>Allergy</addtitle><description>Background:
MicroRNAs (miRNAs) are known to regulate the inflammatory response in various cell types. However, the ability of miRNAs to modulate dendritic cells (DCs) function for allergen immunotherapy is unclear.
Objective:
To assess the role of miR‐23b in the regulation of ovalbumin (OVA)‐induced DC differentiation and function and to investigate the related molecular mechanisms.
Methods:
Bone marrow‐derived dendritic cells (BMDCs) were generated from murine bone marrow progenitor cells and subsequently stimulated with OVA to examine the profile of miRNA expression. After transfection with miR‐23b reagents, DCs were evaluated for endocytic ability, surface marker expression, cytokine secretion and CD4+ T‐cell differentiation. The possible roles of the Notch and NF‐κB signalling pathways were also evaluated. Human monocyte‐derived dendritic cells (MDDCs) were similarly evaluated as well.
Results:
Significant upregulation of miR‐23b was observed in BMDCs pulsed with OVA. Following miR‐23b transfection, BMDCs showed decreased OVA uptake, increased IL‐10 production, decreased IL‐12 production and an enhanced capacity to promote FoxP3+ CD4+ T regulatory cells (Tregs) differentiation. In addition, inactivation of the Notch1 and NF‐κB signalling pathways were observed. Conversely, inhibition of miR‐23b in BMDCs resulted in the opposite effects. In human MDDCs, miRNA23b transfection similarly increased IL‐10 and decreased IL‐12 production, and that treated human MDDCs induced increased FoxP3+ CD4+ T cells.
Conclusion:
Our findings provide evidence that miR‐23b is capable of inducing tolerogenic DC activity and Treg responses in vitro through the inhibition of the Notch1 and NF‐κB signalling pathways; thus, miR‐23b might represent a therapeutic target for the management of allergic diseases.</description><subject>Allergens</subject><subject>Allergens - administration & dosage</subject><subject>Allergens - immunology</subject><subject>Allergic diseases</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone marrow</subject><subject>Bone Marrow Cells - immunology</subject><subject>CD4 antigen</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - cytology</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - metabolism</subject><subject>Dermatology</subject><subject>Differentiation</subject><subject>Foxp3 protein</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Hypersensitivity - immunology</subject><subject>Hypersensitivity - therapy</subject><subject>Immune Tolerance</subject><subject>Immunoregulation</subject><subject>Immunotherapy</subject><subject>in vitro</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Interleukin 12</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>microRNAs</subject><subject>MicroRNAs - immunology</subject><subject>MicroRNAs - metabolism</subject><subject>MicroRNAs - pharmacology</subject><subject>miRNA</subject><subject>Molecular modelling</subject><subject>Monocytes</subject><subject>NF- Kappa B protein</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-κB</subject><subject>Notch</subject><subject>Notch protein</subject><subject>Osteoprogenitor cells</subject><subject>Ovalbumin</subject><subject>Ovalbumin - administration & dosage</subject><subject>Ovalbumin - immunology</subject><subject>Receptor, Notch1 - antagonists & inhibitors</subject><subject>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>signalling pathway</subject><subject>Surface markers</subject><subject>T regulatory cells</subject><subject>Transfection</subject><subject>Up-Regulation</subject><issn>0105-4538</issn><issn>1398-9995</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc2O0zAUhS0EYsrAK6BsEKtk_BPb8YJFp2JmkEKR0KBKbCw3dhqXNC62y7SLeTEegmfCoaVsuRtb53z36toHgAzBAqW6WheIiCoXQtACQ4QKiDlnxf4JmJyNp2ACEaR5SUl1AV6EsIYQcizgc3CBUwmO2AQ8frSNd5_n0xyTZbb1buOiCVl0vfFuZQbbjOLW-GiT7NpMm0F7G5PemL4PmR2yHzZ6l8XOu92qS0JnlwkYVtncxaZDV_Ob_NfP6yzY1aD6fjS2KnYP6hBegmet6oN5dTovwZeb9_ezu7z-dPthNq1zi7lgOeO4aqHWhuIWc80Y1LQqG4wUFcpwTVkJDeMUUogrpsplSUrdEGw0JQK3hFyCt8e56S3fdyZEubFh3F8Nxu2CFJhVFYfwf0hUYiYYTuTrE7lbboyWW283yh_k379NwJsToEKj-tarobHhH0cZxZDAxL07cg-2N4ezj6Acs5ZrOUYqx0jlmLX8k7Xcy2ldj7fUnx_7bYhmf-5X_ptknHAqF_NbWd8vFvz66ywN-w0bsax6</recordid><startdate>201203</startdate><enddate>201203</enddate><creator>Zheng, J.</creator><creator>Jiang, H.-Y.</creator><creator>Li, J.</creator><creator>Tang, H.-C.</creator><creator>Zhang, X.-M.</creator><creator>Wang, X.-R.</creator><creator>Du, J.-T.</creator><creator>Li, H.-B.</creator><creator>Xu, G.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>201203</creationdate><title>MicroRNA-23b promotes tolerogenic properties of dendritic cells in vitro through inhibiting Notch1/NF-κB signalling pathways</title><author>Zheng, J. ; Jiang, H.-Y. ; Li, J. ; Tang, H.-C. ; Zhang, X.-M. ; Wang, X.-R. ; Du, J.-T. ; Li, H.-B. ; Xu, G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i2796-6728f0dde52f27d660d584c21a59ae7d5640e675050286a4b434dc32ed5392f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Allergens</topic><topic>Allergens - administration & dosage</topic><topic>Allergens - immunology</topic><topic>Allergic diseases</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone marrow</topic><topic>Bone Marrow Cells - immunology</topic><topic>CD4 antigen</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - cytology</topic><topic>Dendritic Cells - immunology</topic><topic>Dendritic Cells - metabolism</topic><topic>Dermatology</topic><topic>Differentiation</topic><topic>Foxp3 protein</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Hypersensitivity - immunology</topic><topic>Hypersensitivity - therapy</topic><topic>Immune Tolerance</topic><topic>Immunoregulation</topic><topic>Immunotherapy</topic><topic>in vitro</topic><topic>Inflammation</topic><topic>Interleukin 10</topic><topic>Interleukin 12</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>microRNAs</topic><topic>MicroRNAs - immunology</topic><topic>MicroRNAs - metabolism</topic><topic>MicroRNAs - pharmacology</topic><topic>miRNA</topic><topic>Molecular modelling</topic><topic>Monocytes</topic><topic>NF- Kappa B protein</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-κB</topic><topic>Notch</topic><topic>Notch protein</topic><topic>Osteoprogenitor cells</topic><topic>Ovalbumin</topic><topic>Ovalbumin - administration & dosage</topic><topic>Ovalbumin - immunology</topic><topic>Receptor, Notch1 - antagonists & inhibitors</topic><topic>Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>signalling pathway</topic><topic>Surface markers</topic><topic>T regulatory cells</topic><topic>Transfection</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, J.</creatorcontrib><creatorcontrib>Jiang, H.-Y.</creatorcontrib><creatorcontrib>Li, J.</creatorcontrib><creatorcontrib>Tang, H.-C.</creatorcontrib><creatorcontrib>Zhang, X.-M.</creatorcontrib><creatorcontrib>Wang, X.-R.</creatorcontrib><creatorcontrib>Du, J.-T.</creatorcontrib><creatorcontrib>Li, H.-B.</creatorcontrib><creatorcontrib>Xu, G.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Allergy (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, J.</au><au>Jiang, H.-Y.</au><au>Li, J.</au><au>Tang, H.-C.</au><au>Zhang, X.-M.</au><au>Wang, X.-R.</au><au>Du, J.-T.</au><au>Li, H.-B.</au><au>Xu, G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-23b promotes tolerogenic properties of dendritic cells in vitro through inhibiting Notch1/NF-κB signalling pathways</atitle><jtitle>Allergy (Copenhagen)</jtitle><addtitle>Allergy</addtitle><date>2012-03</date><risdate>2012</risdate><volume>67</volume><issue>3</issue><spage>362</spage><epage>370</epage><pages>362-370</pages><issn>0105-4538</issn><eissn>1398-9995</eissn><coden>LLRGDY</coden><abstract>Background:
MicroRNAs (miRNAs) are known to regulate the inflammatory response in various cell types. However, the ability of miRNAs to modulate dendritic cells (DCs) function for allergen immunotherapy is unclear.
Objective:
To assess the role of miR‐23b in the regulation of ovalbumin (OVA)‐induced DC differentiation and function and to investigate the related molecular mechanisms.
Methods:
Bone marrow‐derived dendritic cells (BMDCs) were generated from murine bone marrow progenitor cells and subsequently stimulated with OVA to examine the profile of miRNA expression. After transfection with miR‐23b reagents, DCs were evaluated for endocytic ability, surface marker expression, cytokine secretion and CD4+ T‐cell differentiation. The possible roles of the Notch and NF‐κB signalling pathways were also evaluated. Human monocyte‐derived dendritic cells (MDDCs) were similarly evaluated as well.
Results:
Significant upregulation of miR‐23b was observed in BMDCs pulsed with OVA. Following miR‐23b transfection, BMDCs showed decreased OVA uptake, increased IL‐10 production, decreased IL‐12 production and an enhanced capacity to promote FoxP3+ CD4+ T regulatory cells (Tregs) differentiation. In addition, inactivation of the Notch1 and NF‐κB signalling pathways were observed. Conversely, inhibition of miR‐23b in BMDCs resulted in the opposite effects. In human MDDCs, miRNA23b transfection similarly increased IL‐10 and decreased IL‐12 production, and that treated human MDDCs induced increased FoxP3+ CD4+ T cells.
Conclusion:
Our findings provide evidence that miR‐23b is capable of inducing tolerogenic DC activity and Treg responses in vitro through the inhibition of the Notch1 and NF‐κB signalling pathways; thus, miR‐23b might represent a therapeutic target for the management of allergic diseases.</abstract><cop>Oxford</cop><pub>Blackwell Publishing Ltd</pub><pmid>22229716</pmid><doi>10.1111/j.1398-9995.2011.02776.x</doi><tpages>9</tpages></addata></record> |
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| ispartof | Allergy (Copenhagen), 2012-03, Vol.67 (3), p.362-370 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Free Content |
| subjects | Allergens Allergens - administration & dosage Allergens - immunology Allergic diseases Animals Biological and medical sciences Bone marrow Bone Marrow Cells - immunology CD4 antigen Cell Differentiation Cells, Cultured Dendritic cells Dendritic Cells - cytology Dendritic Cells - immunology Dendritic Cells - metabolism Dermatology Differentiation Foxp3 protein Fundamental and applied biological sciences. Psychology Fundamental immunology Gene expression Humans Hypersensitivity - immunology Hypersensitivity - therapy Immune Tolerance Immunoregulation Immunotherapy in vitro Inflammation Interleukin 10 Interleukin 12 Lymphocytes T Male Medical sciences Mice Mice, Inbred BALB C microRNAs MicroRNAs - immunology MicroRNAs - metabolism MicroRNAs - pharmacology miRNA Molecular modelling Monocytes NF- Kappa B protein NF-kappa B - antagonists & inhibitors NF-κB Notch Notch protein Osteoprogenitor cells Ovalbumin Ovalbumin - administration & dosage Ovalbumin - immunology Receptor, Notch1 - antagonists & inhibitors Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Signal transduction Signal Transduction - drug effects signalling pathway Surface markers T regulatory cells Transfection Up-Regulation |
| title | MicroRNA-23b promotes tolerogenic properties of dendritic cells in vitro through inhibiting Notch1/NF-κB signalling pathways |
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