CD69 controls the uptake of L-tryptophan through LAT1-CD98 and AhR-dependent secretion of IL-22 in psoriasis
Sanchez-Madrid and colleagues show that CD69 associates with the amino acid transporter LAT1-CD98 to control the uptake of tryptophan and AhR-dependent secretion of IL-22 by skin γδ T cells. The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydro...
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| Veröffentlicht in: | Nature immunology 2016-08, Vol.17 (8), p.985-996 |
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| creator | Cibrian, Danay Saiz, María Laura de la Fuente, Hortensia Sánchez-Díaz, Raquel Moreno-Gonzalo, Olga Jorge, Inmaculada Ferrarini, Alessia Vázquez, Jesús Punzón, Carmen Fresno, Manuel Vicente-Manzanares, Miguel Daudén, Esteban Fernández-Salguero, Pedro M Martín, Pilar Sánchez-Madrid, Francisco |
| description | Sanchez-Madrid and colleagues show that CD69 associates with the amino acid transporter LAT1-CD98 to control the uptake of tryptophan and AhR-dependent secretion of IL-22 by skin γδ T cells.
The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydrocarbon receptor (AhR)-dependent secretion of interleukin 22 (IL-22) by γδ T cells, which contributed to the development of psoriasis induced by IL-23. CD69 associated with the aromatic-amino-acid-transporter complex LAT1-CD98 and regulated its surface expression and uptake of L-tryptophan (L-Trp) and the intracellular quantity of L-Trp-derived activators of AhR.
In vivo
administration of L-Trp, an inhibitor of AhR or IL-22 abrogated the differences between CD69-deficient mice and wild-type mice in skin inflammation. We also observed LAT1-mediated regulation of AhR activation and IL-22 secretion in circulating V
γ
9
+
γδ T cells of psoriatic patients. Thus, CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98-mediated metabolic cues. |
| doi_str_mv | 10.1038/ni.3504 |
| format | Article |
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The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydrocarbon receptor (AhR)-dependent secretion of interleukin 22 (IL-22) by γδ T cells, which contributed to the development of psoriasis induced by IL-23. CD69 associated with the aromatic-amino-acid-transporter complex LAT1-CD98 and regulated its surface expression and uptake of L-tryptophan (L-Trp) and the intracellular quantity of L-Trp-derived activators of AhR.
In vivo
administration of L-Trp, an inhibitor of AhR or IL-22 abrogated the differences between CD69-deficient mice and wild-type mice in skin inflammation. We also observed LAT1-mediated regulation of AhR activation and IL-22 secretion in circulating V
γ
9
+
γδ T cells of psoriatic patients. Thus, CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98-mediated metabolic cues.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/ni.3504</identifier><identifier>PMID: 27376471</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>13/31 ; 45/77 ; 631/250/249/1313/1758 ; 692/420/256/2515 ; 82/51 ; 82/58 ; 96/21 ; 96/95 ; Amino Acid Transport System y+ - metabolism ; Amino Acid Transport System y+L ; Analysis ; Animals ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Antigens, Differentiation, T-Lymphocyte - genetics ; Antigens, Differentiation, T-Lymphocyte - metabolism ; Biomedicine ; Care and treatment ; Cells, Cultured ; Endocytosis ; Fusion Regulatory Protein-1 - metabolism ; Immunology ; Infectious Diseases ; Interleukin-22 ; Interleukin-23 - immunology ; Interleukins ; Interleukins - metabolism ; Lectins, C-Type - genetics ; Lectins, C-Type - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Psoriasis ; Psoriasis - immunology ; Receptors, Antigen, T-Cell, gamma-delta - metabolism ; Receptors, Aryl Hydrocarbon - metabolism ; Skin - immunology ; Skin diseases ; T cells ; T-Lymphocyte Subsets - immunology ; Th17 Cells - immunology ; Tryptophan - metabolism</subject><ispartof>Nature immunology, 2016-08, Vol.17 (8), p.985-996</ispartof><rights>Springer Nature America, Inc. 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Aug 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c575t-50713a4ec7de7d0c5864664b7452d31dd3d8ec9f3c22916ec2e7ced076cf1d923</citedby><cites>FETCH-LOGICAL-c575t-50713a4ec7de7d0c5864664b7452d31dd3d8ec9f3c22916ec2e7ced076cf1d923</cites><orcidid>0000-0002-2392-1764</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/ni.3504$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/ni.3504$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27376471$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cibrian, Danay</creatorcontrib><creatorcontrib>Saiz, María Laura</creatorcontrib><creatorcontrib>de la Fuente, Hortensia</creatorcontrib><creatorcontrib>Sánchez-Díaz, Raquel</creatorcontrib><creatorcontrib>Moreno-Gonzalo, Olga</creatorcontrib><creatorcontrib>Jorge, Inmaculada</creatorcontrib><creatorcontrib>Ferrarini, Alessia</creatorcontrib><creatorcontrib>Vázquez, Jesús</creatorcontrib><creatorcontrib>Punzón, Carmen</creatorcontrib><creatorcontrib>Fresno, Manuel</creatorcontrib><creatorcontrib>Vicente-Manzanares, Miguel</creatorcontrib><creatorcontrib>Daudén, Esteban</creatorcontrib><creatorcontrib>Fernández-Salguero, Pedro M</creatorcontrib><creatorcontrib>Martín, Pilar</creatorcontrib><creatorcontrib>Sánchez-Madrid, Francisco</creatorcontrib><title>CD69 controls the uptake of L-tryptophan through LAT1-CD98 and AhR-dependent secretion of IL-22 in psoriasis</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><addtitle>Nat Immunol</addtitle><description>Sanchez-Madrid and colleagues show that CD69 associates with the amino acid transporter LAT1-CD98 to control the uptake of tryptophan and AhR-dependent secretion of IL-22 by skin γδ T cells.
The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydrocarbon receptor (AhR)-dependent secretion of interleukin 22 (IL-22) by γδ T cells, which contributed to the development of psoriasis induced by IL-23. CD69 associated with the aromatic-amino-acid-transporter complex LAT1-CD98 and regulated its surface expression and uptake of L-tryptophan (L-Trp) and the intracellular quantity of L-Trp-derived activators of AhR.
In vivo
administration of L-Trp, an inhibitor of AhR or IL-22 abrogated the differences between CD69-deficient mice and wild-type mice in skin inflammation. We also observed LAT1-mediated regulation of AhR activation and IL-22 secretion in circulating V
γ
9
+
γδ T cells of psoriatic patients. Thus, CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98-mediated metabolic cues.</description><subject>13/31</subject><subject>45/77</subject><subject>631/250/249/1313/1758</subject><subject>692/420/256/2515</subject><subject>82/51</subject><subject>82/58</subject><subject>96/21</subject><subject>96/95</subject><subject>Amino Acid Transport System y+ - metabolism</subject><subject>Amino Acid Transport System y+L</subject><subject>Analysis</subject><subject>Animals</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, Differentiation, T-Lymphocyte - genetics</subject><subject>Antigens, Differentiation, T-Lymphocyte - metabolism</subject><subject>Biomedicine</subject><subject>Care and treatment</subject><subject>Cells, Cultured</subject><subject>Endocytosis</subject><subject>Fusion Regulatory Protein-1 - metabolism</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><subject>Interleukin-22</subject><subject>Interleukin-23 - 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metabolism</topic><topic>Skin - immunology</topic><topic>Skin diseases</topic><topic>T cells</topic><topic>T-Lymphocyte Subsets - immunology</topic><topic>Th17 Cells - immunology</topic><topic>Tryptophan - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cibrian, Danay</creatorcontrib><creatorcontrib>Saiz, María Laura</creatorcontrib><creatorcontrib>de la Fuente, Hortensia</creatorcontrib><creatorcontrib>Sánchez-Díaz, Raquel</creatorcontrib><creatorcontrib>Moreno-Gonzalo, Olga</creatorcontrib><creatorcontrib>Jorge, Inmaculada</creatorcontrib><creatorcontrib>Ferrarini, Alessia</creatorcontrib><creatorcontrib>Vázquez, Jesús</creatorcontrib><creatorcontrib>Punzón, Carmen</creatorcontrib><creatorcontrib>Fresno, Manuel</creatorcontrib><creatorcontrib>Vicente-Manzanares, Miguel</creatorcontrib><creatorcontrib>Daudén, Esteban</creatorcontrib><creatorcontrib>Fernández-Salguero, Pedro M</creatorcontrib><creatorcontrib>Martín, Pilar</creatorcontrib><creatorcontrib>Sánchez-Madrid, Francisco</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS 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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Nature immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cibrian, Danay</au><au>Saiz, María Laura</au><au>de la Fuente, Hortensia</au><au>Sánchez-Díaz, Raquel</au><au>Moreno-Gonzalo, Olga</au><au>Jorge, Inmaculada</au><au>Ferrarini, Alessia</au><au>Vázquez, Jesús</au><au>Punzón, Carmen</au><au>Fresno, Manuel</au><au>Vicente-Manzanares, Miguel</au><au>Daudén, Esteban</au><au>Fernández-Salguero, Pedro M</au><au>Martín, Pilar</au><au>Sánchez-Madrid, Francisco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD69 controls the uptake of L-tryptophan through LAT1-CD98 and AhR-dependent secretion of IL-22 in psoriasis</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><addtitle>Nat Immunol</addtitle><date>2016-08-01</date><risdate>2016</risdate><volume>17</volume><issue>8</issue><spage>985</spage><epage>996</epage><pages>985-996</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>Sanchez-Madrid and colleagues show that CD69 associates with the amino acid transporter LAT1-CD98 to control the uptake of tryptophan and AhR-dependent secretion of IL-22 by skin γδ T cells.
The activation marker CD69 is expressed by skin γδ T cells. Here we found that CD69 controlled the aryl hydrocarbon receptor (AhR)-dependent secretion of interleukin 22 (IL-22) by γδ T cells, which contributed to the development of psoriasis induced by IL-23. CD69 associated with the aromatic-amino-acid-transporter complex LAT1-CD98 and regulated its surface expression and uptake of L-tryptophan (L-Trp) and the intracellular quantity of L-Trp-derived activators of AhR.
In vivo
administration of L-Trp, an inhibitor of AhR or IL-22 abrogated the differences between CD69-deficient mice and wild-type mice in skin inflammation. We also observed LAT1-mediated regulation of AhR activation and IL-22 secretion in circulating V
γ
9
+
γδ T cells of psoriatic patients. Thus, CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98-mediated metabolic cues.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>27376471</pmid><doi>10.1038/ni.3504</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-2392-1764</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Nature immunology, 2016-08, Vol.17 (8), p.985-996 |
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| source | MEDLINE; SpringerLink Journals; Nature Journals Online |
| subjects | 13/31 45/77 631/250/249/1313/1758 692/420/256/2515 82/51 82/58 96/21 96/95 Amino Acid Transport System y+ - metabolism Amino Acid Transport System y+L Analysis Animals Antigens, CD - genetics Antigens, CD - metabolism Antigens, Differentiation, T-Lymphocyte - genetics Antigens, Differentiation, T-Lymphocyte - metabolism Biomedicine Care and treatment Cells, Cultured Endocytosis Fusion Regulatory Protein-1 - metabolism Immunology Infectious Diseases Interleukin-22 Interleukin-23 - immunology Interleukins Interleukins - metabolism Lectins, C-Type - genetics Lectins, C-Type - metabolism Mice Mice, Inbred C57BL Mice, Knockout Psoriasis Psoriasis - immunology Receptors, Antigen, T-Cell, gamma-delta - metabolism Receptors, Aryl Hydrocarbon - metabolism Skin - immunology Skin diseases T cells T-Lymphocyte Subsets - immunology Th17 Cells - immunology Tryptophan - metabolism |
| title | CD69 controls the uptake of L-tryptophan through LAT1-CD98 and AhR-dependent secretion of IL-22 in psoriasis |
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