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CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity
Th17 cells play a critical role in host defense against extracellular pathogens and tissue homeostasis but can induce autoimmunity. The mechanisms implicated in balancing “pathogenic” and “non-pathogenic” Th17 cell states remain largely unknown. We used single-cell RNA-seq to identify CD5L/AIM as a...
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| Published in: | Cell 2015-12, Vol.163 (6), p.1413-1427 |
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| creator | Wang, Chao Yosef, Nir Gaublomme, Jellert Wu, Chuan Lee, Youjin Clish, Clary B. Kaminski, Jim Xiao, Sheng Zu Horste, Gerd Meyer Pawlak, Mathias Kishi, Yasuhiro Joller, Nicole Karwacz, Katarzyna Zhu, Chen Ordovas-Montanes, Maria Madi, Asaf Wortman, Ivo Miyazaki, Toru Sobel, Raymond A. Park, Hongkun Regev, Aviv Kuchroo, Vijay K. |
| description | Th17 cells play a critical role in host defense against extracellular pathogens and tissue homeostasis but can induce autoimmunity. The mechanisms implicated in balancing “pathogenic” and “non-pathogenic” Th17 cell states remain largely unknown. We used single-cell RNA-seq to identify CD5L/AIM as a regulator expressed in non-pathogenic, but not in pathogenic Th17 cells. Although CD5L does not affect Th17 differentiation, it is a functional switch that regulates the pathogenicity of Th17 cells. Loss of CD5L converts non-pathogenic Th17 cells into pathogenic cells that induce autoimmunity. CD5L mediates this effect by modulating the intracellular lipidome, altering fatty acid composition and restricting cholesterol biosynthesis and, thus, ligand availability for Rorγt, the master transcription factor of Th17 cells. Our study identifies CD5L as a critical regulator of the Th17 cell functional state and highlights the importance of lipid metabolism in balancing immune protection and disease induced by T cells.
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•CD5L is preferentially expressed in non-pathogenic Th17 cells•CD5L is a major switch of Th17 cell functional states in vivo•CD5L regulates T cell lipidome in correlation with Th17 cell function•CD5L alters T cell function through PUFA/SFA balance and Rorγt ligand availability
CD5L operates as a critical switch of Th17 cells functional states, regulating their ability to cause disease through changes in lipid metabolism and function of the master transcription factor Rorγt. |
| doi_str_mv | 10.1016/j.cell.2015.10.068 |
| format | article |
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[Display omitted]
•CD5L is preferentially expressed in non-pathogenic Th17 cells•CD5L is a major switch of Th17 cell functional states in vivo•CD5L regulates T cell lipidome in correlation with Th17 cell function•CD5L alters T cell function through PUFA/SFA balance and Rorγt ligand availability
CD5L operates as a critical switch of Th17 cells functional states, regulating their ability to cause disease through changes in lipid metabolism and function of the master transcription factor Rorγt.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/j.cell.2015.10.068</identifier><identifier>PMID: 26607793</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Apoptosis Regulatory Proteins - metabolism ; Cell Differentiation ; Central Nervous System - pathology ; Cholesterol - biosynthesis ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Fatty Acids, Unsaturated - metabolism ; Humans ; Lipid Metabolism ; Lymph Nodes - pathology ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism ; Receptor Tyrosine Kinase-like Orphan Receptors - metabolism ; Receptors, Immunologic - metabolism ; Receptors, Scavenger ; Single-Cell Analysis ; Th17 Cells - immunology ; Th17 Cells - pathology</subject><ispartof>Cell, 2015-12, Vol.163 (6), p.1413-1427</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-f0728613f4c53cccb4b3323a82a9811e9c588f2ca3ab393ca5784b404c838b7a3</citedby><cites>FETCH-LOGICAL-c470t-f0728613f4c53cccb4b3323a82a9811e9c588f2ca3ab393ca5784b404c838b7a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26607793$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Yosef, Nir</creatorcontrib><creatorcontrib>Gaublomme, Jellert</creatorcontrib><creatorcontrib>Wu, Chuan</creatorcontrib><creatorcontrib>Lee, Youjin</creatorcontrib><creatorcontrib>Clish, Clary B.</creatorcontrib><creatorcontrib>Kaminski, Jim</creatorcontrib><creatorcontrib>Xiao, Sheng</creatorcontrib><creatorcontrib>Zu Horste, Gerd Meyer</creatorcontrib><creatorcontrib>Pawlak, Mathias</creatorcontrib><creatorcontrib>Kishi, Yasuhiro</creatorcontrib><creatorcontrib>Joller, Nicole</creatorcontrib><creatorcontrib>Karwacz, Katarzyna</creatorcontrib><creatorcontrib>Zhu, Chen</creatorcontrib><creatorcontrib>Ordovas-Montanes, Maria</creatorcontrib><creatorcontrib>Madi, Asaf</creatorcontrib><creatorcontrib>Wortman, Ivo</creatorcontrib><creatorcontrib>Miyazaki, Toru</creatorcontrib><creatorcontrib>Sobel, Raymond A.</creatorcontrib><creatorcontrib>Park, Hongkun</creatorcontrib><creatorcontrib>Regev, Aviv</creatorcontrib><creatorcontrib>Kuchroo, Vijay K.</creatorcontrib><title>CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity</title><title>Cell</title><addtitle>Cell</addtitle><description>Th17 cells play a critical role in host defense against extracellular pathogens and tissue homeostasis but can induce autoimmunity. The mechanisms implicated in balancing “pathogenic” and “non-pathogenic” Th17 cell states remain largely unknown. We used single-cell RNA-seq to identify CD5L/AIM as a regulator expressed in non-pathogenic, but not in pathogenic Th17 cells. Although CD5L does not affect Th17 differentiation, it is a functional switch that regulates the pathogenicity of Th17 cells. Loss of CD5L converts non-pathogenic Th17 cells into pathogenic cells that induce autoimmunity. CD5L mediates this effect by modulating the intracellular lipidome, altering fatty acid composition and restricting cholesterol biosynthesis and, thus, ligand availability for Rorγt, the master transcription factor of Th17 cells. Our study identifies CD5L as a critical regulator of the Th17 cell functional state and highlights the importance of lipid metabolism in balancing immune protection and disease induced by T cells.
[Display omitted]
•CD5L is preferentially expressed in non-pathogenic Th17 cells•CD5L is a major switch of Th17 cell functional states in vivo•CD5L regulates T cell lipidome in correlation with Th17 cell function•CD5L alters T cell function through PUFA/SFA balance and Rorγt ligand availability
CD5L operates as a critical switch of Th17 cells functional states, regulating their ability to cause disease through changes in lipid metabolism and function of the master transcription factor Rorγt.</description><subject>Animals</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Cell Differentiation</subject><subject>Central Nervous System - pathology</subject><subject>Cholesterol - biosynthesis</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Fatty Acids, Unsaturated - metabolism</subject><subject>Humans</subject><subject>Lipid Metabolism</subject><subject>Lymph Nodes - pathology</subject><subject>Mice</subject><subject>Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism</subject><subject>Receptor Tyrosine Kinase-like Orphan Receptors - metabolism</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Receptors, Scavenger</subject><subject>Single-Cell Analysis</subject><subject>Th17 Cells - immunology</subject><subject>Th17 Cells - pathology</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNp9kMlOwzAURS0EomX4ARYoSzZJPcaOxKaEqSIIhMrachynddUmxU6Q-vc4amHJytLTuff5HQCuEEwQROlklWizXicYIhYGCUzFERgjmPGYIo6PwRjCDMci5XQEzrxfQQgFY-wUjHCaQs4zMgYv-T0rJtPZa_RhFv1adcZHhd3aKrqzrd813dJ46yPVVAHwnVO28dF8iXiUh93Ru-qW7cI0VttudwFOarX25vLwnoPPx4d5_hwXb0-zfFrEmnLYxTXkWKSI1FQzorUuaUkIJkpglQmETKaZEDXWiqiSZEQrxgUtKaRaEFFyRc7Bzb5369qvPvxKbqwfVKjGtL2XiNNUcCR4GlC8R7VrvXemlltnN8rtJIJykChXckjKQeIwCxJD6PrQ35cbU_1Ffq0F4HYPmHDltzVOem1No01lndGdrFr7X_8PPLqBHg</recordid><startdate>20151203</startdate><enddate>20151203</enddate><creator>Wang, Chao</creator><creator>Yosef, Nir</creator><creator>Gaublomme, Jellert</creator><creator>Wu, Chuan</creator><creator>Lee, Youjin</creator><creator>Clish, Clary B.</creator><creator>Kaminski, Jim</creator><creator>Xiao, Sheng</creator><creator>Zu Horste, Gerd Meyer</creator><creator>Pawlak, Mathias</creator><creator>Kishi, Yasuhiro</creator><creator>Joller, Nicole</creator><creator>Karwacz, Katarzyna</creator><creator>Zhu, Chen</creator><creator>Ordovas-Montanes, Maria</creator><creator>Madi, Asaf</creator><creator>Wortman, Ivo</creator><creator>Miyazaki, Toru</creator><creator>Sobel, Raymond A.</creator><creator>Park, Hongkun</creator><creator>Regev, Aviv</creator><creator>Kuchroo, Vijay K.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>7X8</scope></search><sort><creationdate>20151203</creationdate><title>CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity</title><author>Wang, Chao ; Yosef, Nir ; Gaublomme, Jellert ; Wu, Chuan ; Lee, Youjin ; Clish, Clary B. ; Kaminski, Jim ; Xiao, Sheng ; Zu Horste, Gerd Meyer ; Pawlak, Mathias ; Kishi, Yasuhiro ; Joller, Nicole ; Karwacz, Katarzyna ; Zhu, Chen ; Ordovas-Montanes, Maria ; Madi, Asaf ; Wortman, Ivo ; Miyazaki, Toru ; Sobel, Raymond A. ; Park, Hongkun ; Regev, Aviv ; Kuchroo, Vijay K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-f0728613f4c53cccb4b3323a82a9811e9c588f2ca3ab393ca5784b404c838b7a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Cell Differentiation</topic><topic>Central Nervous System - pathology</topic><topic>Cholesterol - biosynthesis</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Fatty Acids, Unsaturated - metabolism</topic><topic>Humans</topic><topic>Lipid Metabolism</topic><topic>Lymph Nodes - pathology</topic><topic>Mice</topic><topic>Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism</topic><topic>Receptor Tyrosine Kinase-like Orphan Receptors - metabolism</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Receptors, Scavenger</topic><topic>Single-Cell Analysis</topic><topic>Th17 Cells - immunology</topic><topic>Th17 Cells - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Yosef, Nir</creatorcontrib><creatorcontrib>Gaublomme, Jellert</creatorcontrib><creatorcontrib>Wu, Chuan</creatorcontrib><creatorcontrib>Lee, Youjin</creatorcontrib><creatorcontrib>Clish, Clary B.</creatorcontrib><creatorcontrib>Kaminski, Jim</creatorcontrib><creatorcontrib>Xiao, Sheng</creatorcontrib><creatorcontrib>Zu Horste, Gerd Meyer</creatorcontrib><creatorcontrib>Pawlak, Mathias</creatorcontrib><creatorcontrib>Kishi, Yasuhiro</creatorcontrib><creatorcontrib>Joller, Nicole</creatorcontrib><creatorcontrib>Karwacz, Katarzyna</creatorcontrib><creatorcontrib>Zhu, Chen</creatorcontrib><creatorcontrib>Ordovas-Montanes, Maria</creatorcontrib><creatorcontrib>Madi, Asaf</creatorcontrib><creatorcontrib>Wortman, Ivo</creatorcontrib><creatorcontrib>Miyazaki, Toru</creatorcontrib><creatorcontrib>Sobel, Raymond A.</creatorcontrib><creatorcontrib>Park, Hongkun</creatorcontrib><creatorcontrib>Regev, Aviv</creatorcontrib><creatorcontrib>Kuchroo, Vijay K.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Chao</au><au>Yosef, Nir</au><au>Gaublomme, Jellert</au><au>Wu, Chuan</au><au>Lee, Youjin</au><au>Clish, Clary B.</au><au>Kaminski, Jim</au><au>Xiao, Sheng</au><au>Zu Horste, Gerd Meyer</au><au>Pawlak, Mathias</au><au>Kishi, Yasuhiro</au><au>Joller, Nicole</au><au>Karwacz, Katarzyna</au><au>Zhu, Chen</au><au>Ordovas-Montanes, Maria</au><au>Madi, Asaf</au><au>Wortman, Ivo</au><au>Miyazaki, Toru</au><au>Sobel, Raymond A.</au><au>Park, Hongkun</au><au>Regev, Aviv</au><au>Kuchroo, Vijay K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>2015-12-03</date><risdate>2015</risdate><volume>163</volume><issue>6</issue><spage>1413</spage><epage>1427</epage><pages>1413-1427</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Th17 cells play a critical role in host defense against extracellular pathogens and tissue homeostasis but can induce autoimmunity. The mechanisms implicated in balancing “pathogenic” and “non-pathogenic” Th17 cell states remain largely unknown. We used single-cell RNA-seq to identify CD5L/AIM as a regulator expressed in non-pathogenic, but not in pathogenic Th17 cells. Although CD5L does not affect Th17 differentiation, it is a functional switch that regulates the pathogenicity of Th17 cells. Loss of CD5L converts non-pathogenic Th17 cells into pathogenic cells that induce autoimmunity. CD5L mediates this effect by modulating the intracellular lipidome, altering fatty acid composition and restricting cholesterol biosynthesis and, thus, ligand availability for Rorγt, the master transcription factor of Th17 cells. Our study identifies CD5L as a critical regulator of the Th17 cell functional state and highlights the importance of lipid metabolism in balancing immune protection and disease induced by T cells.
[Display omitted]
•CD5L is preferentially expressed in non-pathogenic Th17 cells•CD5L is a major switch of Th17 cell functional states in vivo•CD5L regulates T cell lipidome in correlation with Th17 cell function•CD5L alters T cell function through PUFA/SFA balance and Rorγt ligand availability
CD5L operates as a critical switch of Th17 cells functional states, regulating their ability to cause disease through changes in lipid metabolism and function of the master transcription factor Rorγt.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26607793</pmid><doi>10.1016/j.cell.2015.10.068</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell, 2015-12, Vol.163 (6), p.1413-1427 |
| issn | 0092-8674 1097-4172 |
| language | eng |
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| source | BACON - Elsevier - GLOBAL_SCIENCEDIRECT-OPENACCESS |
| subjects | Animals Apoptosis Regulatory Proteins - metabolism Cell Differentiation Central Nervous System - pathology Cholesterol - biosynthesis Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - pathology Fatty Acids, Unsaturated - metabolism Humans Lipid Metabolism Lymph Nodes - pathology Mice Nuclear Receptor Subfamily 1, Group F, Member 3 - metabolism Receptor Tyrosine Kinase-like Orphan Receptors - metabolism Receptors, Immunologic - metabolism Receptors, Scavenger Single-Cell Analysis Th17 Cells - immunology Th17 Cells - pathology |
| title | CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity |
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