DC activated via dectin-1 convert Treg into IL-17 producers
Th cells producing IL-17 play a pro-inflammatory role at mucosal surfaces. Treg at the same sites dampen inflammation and prevent immunopathology. Th cells producing IL-17 (Th17) and Treg are thought to be distinct populations defined by expression of the transcription factors ROR-γt and Foxp3, resp...
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| Veröffentlicht in: | European journal of immunology 2008-12, Vol.38 (12), p.3274-3281 |
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| container_title | European journal of immunology |
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| creator | Osorio, Fabiola LeibundGut-Landmann, Salomé Lochner, Matthias Lahl, Katharina Sparwasser, Tim Eberl, Gérard Reis e Sousa, Caetano |
| description | Th cells producing IL-17 play a pro-inflammatory role at mucosal surfaces. Treg at the same sites dampen inflammation and prevent immunopathology. Th cells producing IL-17 (Th17) and Treg are thought to be distinct populations defined by expression of the transcription factors ROR-γt and Foxp3, respectively. Here, we show that mouse CD25⁺Foxp3⁺ Treg can be converted into a hybrid T-cell population characterized by the expression of Foxp3 and ROR-γt and the production of IL-17. Conversion was observed upon coculture with DC selectively activated via dectin-1, a C-type lectin receptor involved in fungal recognition, and depended on IL-23 produced by DC. Within the Foxp3⁺ population, only Foxp3⁺ROR-γt⁺ T cells but not Foxp3⁺ROR-γt⁻-T cells become Foxp3⁺IL-17⁺ T cells. These results indicate that some Foxp3⁺ T cells can produce IL-17 while retaining Foxp3 expression and suggest that Treg could play an unexpected pro-inflammatory role in some settings. |
| doi_str_mv | 10.1002/eji.200838950 |
| format | Article |
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Treg at the same sites dampen inflammation and prevent immunopathology. Th cells producing IL-17 (Th17) and Treg are thought to be distinct populations defined by expression of the transcription factors ROR-γt and Foxp3, respectively. Here, we show that mouse CD25⁺Foxp3⁺ Treg can be converted into a hybrid T-cell population characterized by the expression of Foxp3 and ROR-γt and the production of IL-17. Conversion was observed upon coculture with DC selectively activated via dectin-1, a C-type lectin receptor involved in fungal recognition, and depended on IL-23 produced by DC. Within the Foxp3⁺ population, only Foxp3⁺ROR-γt⁺ T cells but not Foxp3⁺ROR-γt⁻-T cells become Foxp3⁺IL-17⁺ T cells. These results indicate that some Foxp3⁺ T cells can produce IL-17 while retaining Foxp3 expression and suggest that Treg could play an unexpected pro-inflammatory role in some settings.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.200838950</identifier><identifier>PMID: 19039774</identifier><language>eng</language><publisher>Weinheim: Wiley-VCH Verlag</publisher><subject>Animals ; Cell Differentiation - immunology ; Dectin‐1 ; Dendritic Cells - drug effects ; Dendritic Cells - immunology ; Forkhead Transcription Factors - immunology ; Highlights ; Interleukin-17 - biosynthesis ; Interleukin-17 - immunology ; Interleukin-2 Receptor alpha Subunit - immunology ; Interleukin-23 - deficiency ; Interleukin-23 - genetics ; Interleukin-23 - metabolism ; Lectins, C-Type ; Membrane Proteins - pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins - pharmacology ; T-Lymphocytes, Regulatory - cytology ; T-Lymphocytes, Regulatory - drug effects ; T-Lymphocytes, Regulatory - immunology ; Th17 ; Treg</subject><ispartof>European journal of immunology, 2008-12, Vol.38 (12), p.3274-3281</ispartof><rights>Copyright © 2008 WILEY‐VCH Verlag GmbH & Co. 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KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4880-fdfc920e0d514e6b6b0a772fe3351adcec2c1e95a897d7ad3969abf1add862a93</citedby><cites>FETCH-LOGICAL-c4880-fdfc920e0d514e6b6b0a772fe3351adcec2c1e95a897d7ad3969abf1add862a93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Feji.200838950$$EPDF$$P50$$Gwiley$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.200838950$$EHTML$$P50$$Gwiley$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19039774$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Osorio, Fabiola</creatorcontrib><creatorcontrib>LeibundGut-Landmann, Salomé</creatorcontrib><creatorcontrib>Lochner, Matthias</creatorcontrib><creatorcontrib>Lahl, Katharina</creatorcontrib><creatorcontrib>Sparwasser, Tim</creatorcontrib><creatorcontrib>Eberl, Gérard</creatorcontrib><creatorcontrib>Reis e Sousa, Caetano</creatorcontrib><title>DC activated via dectin-1 convert Treg into IL-17 producers</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>Th cells producing IL-17 play a pro-inflammatory role at mucosal surfaces. Treg at the same sites dampen inflammation and prevent immunopathology. Th cells producing IL-17 (Th17) and Treg are thought to be distinct populations defined by expression of the transcription factors ROR-γt and Foxp3, respectively. Here, we show that mouse CD25⁺Foxp3⁺ Treg can be converted into a hybrid T-cell population characterized by the expression of Foxp3 and ROR-γt and the production of IL-17. Conversion was observed upon coculture with DC selectively activated via dectin-1, a C-type lectin receptor involved in fungal recognition, and depended on IL-23 produced by DC. Within the Foxp3⁺ population, only Foxp3⁺ROR-γt⁺ T cells but not Foxp3⁺ROR-γt⁻-T cells become Foxp3⁺IL-17⁺ T cells. These results indicate that some Foxp3⁺ T cells can produce IL-17 while retaining Foxp3 expression and suggest that Treg could play an unexpected pro-inflammatory role in some settings.</description><subject>Animals</subject><subject>Cell Differentiation - immunology</subject><subject>Dectin‐1</subject><subject>Dendritic Cells - drug effects</subject><subject>Dendritic Cells - immunology</subject><subject>Forkhead Transcription Factors - immunology</subject><subject>Highlights</subject><subject>Interleukin-17 - biosynthesis</subject><subject>Interleukin-17 - immunology</subject><subject>Interleukin-2 Receptor alpha Subunit - immunology</subject><subject>Interleukin-23 - deficiency</subject><subject>Interleukin-23 - genetics</subject><subject>Interleukin-23 - metabolism</subject><subject>Lectins, C-Type</subject><subject>Membrane Proteins - pharmacology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nerve Tissue Proteins - pharmacology</subject><subject>T-Lymphocytes, Regulatory - cytology</subject><subject>T-Lymphocytes, Regulatory - drug effects</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Th17</subject><subject>Treg</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNqFkU1PGzEQhq2qqAlpj1zbPfW2YWzvrm1VqlSFAEGROABny7FnU0ebdWpvgvj3LCTi41JOI2ueeTTjl5ATCmMKwE5x5ccMQHKpSvhEhrRkNC9oQT-TIQAtcqYkDMhxSisAUFWpvpABVcCVEMWQ_DqbZMZ2fmc6dNnOm8xh_2xzmtnQ7jB22W3EZebbLmSzeU5FtonBbS3G9JUc1aZJ-O1QR-TufHo7uczn1xezyZ95bgspIa9dbRUDBFfSAqtFtQAjBKuR85IaZ9EyS1GVRirhhHFcVcos6r7lZMWM4iPye-_dbBdr7AfaLppGb6Jfm_igg_H6faf1f_Uy7DSrlCoY7wU_D4IY_m0xdXrtk8WmMS2GbdKVkoXk6mOQAWPPnz0i-R60MaQUsX7ZhoJ-ykX3ueiXXHr--9sTXulDED0g9sC9b_Dh_zY9vZq9Vf_YT9YmaLOMPum7GwaUAy0r0SP8Eez6ohc</recordid><startdate>200812</startdate><enddate>200812</enddate><creator>Osorio, Fabiola</creator><creator>LeibundGut-Landmann, Salomé</creator><creator>Lochner, Matthias</creator><creator>Lahl, Katharina</creator><creator>Sparwasser, Tim</creator><creator>Eberl, Gérard</creator><creator>Reis e Sousa, Caetano</creator><general>Wiley-VCH Verlag</general><general>WILEY‐VCH Verlag</general><general>WILEY-VCH Verlag</general><scope>FBQ</scope><scope>24P</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>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200812</creationdate><title>DC activated via dectin-1 convert Treg into IL-17 producers</title><author>Osorio, Fabiola ; 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Treg at the same sites dampen inflammation and prevent immunopathology. Th cells producing IL-17 (Th17) and Treg are thought to be distinct populations defined by expression of the transcription factors ROR-γt and Foxp3, respectively. Here, we show that mouse CD25⁺Foxp3⁺ Treg can be converted into a hybrid T-cell population characterized by the expression of Foxp3 and ROR-γt and the production of IL-17. Conversion was observed upon coculture with DC selectively activated via dectin-1, a C-type lectin receptor involved in fungal recognition, and depended on IL-23 produced by DC. Within the Foxp3⁺ population, only Foxp3⁺ROR-γt⁺ T cells but not Foxp3⁺ROR-γt⁻-T cells become Foxp3⁺IL-17⁺ T cells. These results indicate that some Foxp3⁺ T cells can produce IL-17 while retaining Foxp3 expression and suggest that Treg could play an unexpected pro-inflammatory role in some settings.</abstract><cop>Weinheim</cop><pub>Wiley-VCH Verlag</pub><pmid>19039774</pmid><doi>10.1002/eji.200838950</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | European journal of immunology, 2008-12, Vol.38 (12), p.3274-3281 |
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| source | Wiley Free Content; MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Cell Differentiation - immunology Dectin‐1 Dendritic Cells - drug effects Dendritic Cells - immunology Forkhead Transcription Factors - immunology Highlights Interleukin-17 - biosynthesis Interleukin-17 - immunology Interleukin-2 Receptor alpha Subunit - immunology Interleukin-23 - deficiency Interleukin-23 - genetics Interleukin-23 - metabolism Lectins, C-Type Membrane Proteins - pharmacology Mice Mice, Inbred C57BL Mice, Knockout Nerve Tissue Proteins - pharmacology T-Lymphocytes, Regulatory - cytology T-Lymphocytes, Regulatory - drug effects T-Lymphocytes, Regulatory - immunology Th17 Treg |
| title | DC activated via dectin-1 convert Treg into IL-17 producers |
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