Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93
The interleukin (IL)-17 family, consisting of six members, promotes host defense but can in some context promote the development of autoimmune disease. Here, we examined the role of IL-17D, a poorly understood member in the IL-17 family. IL-17D was expressed primarily by colonic epithelial cells. Il...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2021-04, Vol.54 (4), p.673-686.e4 |
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| creator | Huang, Jinling Lee, Hae-youn Zhao, Xiaohong Han, Jinyi Su, Yang Sun, Qinli Shao, Jing Ge, Jiwan Zhao, Yuxi Bai, Xue He, Yi Wang, Xinquan Wang, Xiaohu Dong, Chen |
| description | The interleukin (IL)-17 family, consisting of six members, promotes host defense but can in some context promote the development of autoimmune disease. Here, we examined the role of IL-17D, a poorly understood member in the IL-17 family. IL-17D was expressed primarily by colonic epithelial cells. Il17d−/− mice were more susceptible to acute colitis, bacterial infection and experimentally induced colon cancer than their wildtype counterparts. Il17d deficiency impaired IL-22 production by group 3 innate lymphoid cells (ILC3s) and reduced expression of IL-22-dependent antimicrobial peptides, RegIIIβ and RegIIIγ, in colon tissue at steady state and in colitis; this was associated with changes in microbial composition and dysbiosis. Protein purification studies revealed that IL-17D bound not canonical IL-17 receptors, but rather CD93, a glycoprotein expressed on mature ILC3s. Mice lacking Cd93 in ILC3s exhibited impaired IL-22 production and aggravated colonic inflammation in experimental colitis. Thus, an IL-17D-CD93 axis regulates ILC3 function to preserve intestinal homeostasis.
[Display omitted]
•IL-17D is required for intestinal hemostasis•IL-17D deficiency results in defective IL-22 production by ILC3s•CD93 is a functional receptor of IL-17D expressed on mature ILC3s•CD93 deficiency decreases ILC3 development and IL-22 production in ILC3s
Among IL-17 cytokines, IL-17D is the least studied member. In this study, Dong et al. demonstrate that intestine epithelial cells-derived IL-17D serve as a critical factor in regulating ILC3s function and intestinal homeostasis by binding the receptor CD93. |
| doi_str_mv | 10.1016/j.immuni.2021.03.018 |
| format | Article |
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[Display omitted]
•IL-17D is required for intestinal hemostasis•IL-17D deficiency results in defective IL-22 production by ILC3s•CD93 is a functional receptor of IL-17D expressed on mature ILC3s•CD93 deficiency decreases ILC3 development and IL-22 production in ILC3s
Among IL-17 cytokines, IL-17D is the least studied member. In this study, Dong et al. demonstrate that intestine epithelial cells-derived IL-17D serve as a critical factor in regulating ILC3s function and intestinal homeostasis by binding the receptor CD93.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2021.03.018</identifier><identifier>PMID: 33852831</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antigens ; Antiinfectives and antibacterials ; Antimicrobial peptides ; Autoimmune diseases ; Bacterial diseases ; Bone marrow ; Cancer ; Cell Line ; Colitis ; Colitis - immunology ; Colon ; Colon - immunology ; Colon cancer ; Colorectal cancer ; Cytokines ; Dysbacteriosis ; Epithelial cells ; Epithelial Cells - immunology ; Epithelium ; Gene expression ; Glycoproteins ; Homeostasis ; Immunity, Innate - immunology ; Inflammation ; Inflammatory bowel disease ; Interleukin 1 ; Interleukin 17 ; Interleukin 22 ; Interleukin-27 - immunology ; Interleukins - immunology ; Intestine ; Lymphocytes ; Lymphocytes - immunology ; Lymphoid cells ; Male ; Membrane Glycoproteins - immunology ; Mice ; Mice, Inbred C57BL ; Microorganisms ; Pathogens ; Peptides ; Physiology ; Protein composition ; Protein purification ; RAW 264.7 Cells ; Receptors ; Rodents ; Roles ; Small intestine ; Thymus gland ; Transcription factors</subject><ispartof>Immunity (Cambridge, Mass.), 2021-04, Vol.54 (4), p.673-686.e4</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><rights>2021. Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c487t-958c0d58f27cf8251edfdcd0ecea43d195a9bc6e32b530755ae09f61cf24a88e3</citedby><cites>FETCH-LOGICAL-c487t-958c0d58f27cf8251edfdcd0ecea43d195a9bc6e32b530755ae09f61cf24a88e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1074761321001308$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33852831$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Jinling</creatorcontrib><creatorcontrib>Lee, Hae-youn</creatorcontrib><creatorcontrib>Zhao, Xiaohong</creatorcontrib><creatorcontrib>Han, Jinyi</creatorcontrib><creatorcontrib>Su, Yang</creatorcontrib><creatorcontrib>Sun, Qinli</creatorcontrib><creatorcontrib>Shao, Jing</creatorcontrib><creatorcontrib>Ge, Jiwan</creatorcontrib><creatorcontrib>Zhao, Yuxi</creatorcontrib><creatorcontrib>Bai, Xue</creatorcontrib><creatorcontrib>He, Yi</creatorcontrib><creatorcontrib>Wang, Xinquan</creatorcontrib><creatorcontrib>Wang, Xiaohu</creatorcontrib><creatorcontrib>Dong, Chen</creatorcontrib><title>Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>The interleukin (IL)-17 family, consisting of six members, promotes host defense but can in some context promote the development of autoimmune disease. Here, we examined the role of IL-17D, a poorly understood member in the IL-17 family. IL-17D was expressed primarily by colonic epithelial cells. Il17d−/− mice were more susceptible to acute colitis, bacterial infection and experimentally induced colon cancer than their wildtype counterparts. Il17d deficiency impaired IL-22 production by group 3 innate lymphoid cells (ILC3s) and reduced expression of IL-22-dependent antimicrobial peptides, RegIIIβ and RegIIIγ, in colon tissue at steady state and in colitis; this was associated with changes in microbial composition and dysbiosis. Protein purification studies revealed that IL-17D bound not canonical IL-17 receptors, but rather CD93, a glycoprotein expressed on mature ILC3s. Mice lacking Cd93 in ILC3s exhibited impaired IL-22 production and aggravated colonic inflammation in experimental colitis. Thus, an IL-17D-CD93 axis regulates ILC3 function to preserve intestinal homeostasis.
[Display omitted]
•IL-17D is required for intestinal hemostasis•IL-17D deficiency results in defective IL-22 production by ILC3s•CD93 is a functional receptor of IL-17D expressed on mature ILC3s•CD93 deficiency decreases ILC3 development and IL-22 production in ILC3s
Among IL-17 cytokines, IL-17D is the least studied member. In this study, Dong et al. demonstrate that intestine epithelial cells-derived IL-17D serve as a critical factor in regulating ILC3s function and intestinal homeostasis by binding the receptor CD93.</description><subject>Animals</subject><subject>Antigens</subject><subject>Antiinfectives and antibacterials</subject><subject>Antimicrobial peptides</subject><subject>Autoimmune diseases</subject><subject>Bacterial diseases</subject><subject>Bone marrow</subject><subject>Cancer</subject><subject>Cell Line</subject><subject>Colitis</subject><subject>Colitis - immunology</subject><subject>Colon</subject><subject>Colon - immunology</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Cytokines</subject><subject>Dysbacteriosis</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - immunology</subject><subject>Epithelium</subject><subject>Gene expression</subject><subject>Glycoproteins</subject><subject>Homeostasis</subject><subject>Immunity, Innate - immunology</subject><subject>Inflammation</subject><subject>Inflammatory bowel disease</subject><subject>Interleukin 1</subject><subject>Interleukin 17</subject><subject>Interleukin 22</subject><subject>Interleukin-27 - immunology</subject><subject>Interleukins - immunology</subject><subject>Intestine</subject><subject>Lymphocytes</subject><subject>Lymphocytes - immunology</subject><subject>Lymphoid cells</subject><subject>Male</subject><subject>Membrane Glycoproteins - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microorganisms</subject><subject>Pathogens</subject><subject>Peptides</subject><subject>Physiology</subject><subject>Protein composition</subject><subject>Protein purification</subject><subject>RAW 264.7 Cells</subject><subject>Receptors</subject><subject>Rodents</subject><subject>Roles</subject><subject>Small intestine</subject><subject>Thymus gland</subject><subject>Transcription factors</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtv1DAURi0Eog_4BwhZYsMmqZ8TZ4OEplAqVWJTFqysjH0z4yGxgx9I_fd1NIUFi658LZ3vu1cHoXeUtJTQzdWxdfNcvGsZYbQlvCVUvUDnlPRdI6giL9e5E023ofwMXaR0JIQK2ZPX6IxzJZni9Bz9vPUZ4gTll_MN7a5xhH2ZhgwJ72MoC-bYeV__eHqYl0NwFhuYJjwWb7ILHudDxfYH7HKqWQNLDhFvr3v-Br0ahynB26f3Ev34-uV--625-35zu_181xihutz0UhlipRpZZ0bFJAU7WmNJrRoEt7SXQ78zG-BsJznppByA9OOGmpGJQSngl-jjqXeJ4XeBlPXs0nrj4CGUpGslZ4ITISr64T_0GEr09bqVYpwpKfpKiRNlYkgpwqiX6OYhPmhK9KpeH_VJvV7Va8J1VV9j75_Ky24G-y_013UFPp0AqDb-OIg6GQfegHVVXNY2uOc3PALqH5ZZ</recordid><startdate>20210413</startdate><enddate>20210413</enddate><creator>Huang, Jinling</creator><creator>Lee, Hae-youn</creator><creator>Zhao, Xiaohong</creator><creator>Han, Jinyi</creator><creator>Su, Yang</creator><creator>Sun, Qinli</creator><creator>Shao, Jing</creator><creator>Ge, Jiwan</creator><creator>Zhao, Yuxi</creator><creator>Bai, Xue</creator><creator>He, Yi</creator><creator>Wang, Xinquan</creator><creator>Wang, Xiaohu</creator><creator>Dong, Chen</creator><general>Elsevier Inc</general><general>Elsevier Limited</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20210413</creationdate><title>Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93</title><author>Huang, Jinling ; 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Here, we examined the role of IL-17D, a poorly understood member in the IL-17 family. IL-17D was expressed primarily by colonic epithelial cells. Il17d−/− mice were more susceptible to acute colitis, bacterial infection and experimentally induced colon cancer than their wildtype counterparts. Il17d deficiency impaired IL-22 production by group 3 innate lymphoid cells (ILC3s) and reduced expression of IL-22-dependent antimicrobial peptides, RegIIIβ and RegIIIγ, in colon tissue at steady state and in colitis; this was associated with changes in microbial composition and dysbiosis. Protein purification studies revealed that IL-17D bound not canonical IL-17 receptors, but rather CD93, a glycoprotein expressed on mature ILC3s. Mice lacking Cd93 in ILC3s exhibited impaired IL-22 production and aggravated colonic inflammation in experimental colitis. Thus, an IL-17D-CD93 axis regulates ILC3 function to preserve intestinal homeostasis.
[Display omitted]
•IL-17D is required for intestinal hemostasis•IL-17D deficiency results in defective IL-22 production by ILC3s•CD93 is a functional receptor of IL-17D expressed on mature ILC3s•CD93 deficiency decreases ILC3 development and IL-22 production in ILC3s
Among IL-17 cytokines, IL-17D is the least studied member. In this study, Dong et al. demonstrate that intestine epithelial cells-derived IL-17D serve as a critical factor in regulating ILC3s function and intestinal homeostasis by binding the receptor CD93.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>33852831</pmid><doi>10.1016/j.immuni.2021.03.018</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | Immunity (Cambridge, Mass.), 2021-04, Vol.54 (4), p.673-686.e4 |
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| subjects | Animals Antigens Antiinfectives and antibacterials Antimicrobial peptides Autoimmune diseases Bacterial diseases Bone marrow Cancer Cell Line Colitis Colitis - immunology Colon Colon - immunology Colon cancer Colorectal cancer Cytokines Dysbacteriosis Epithelial cells Epithelial Cells - immunology Epithelium Gene expression Glycoproteins Homeostasis Immunity, Innate - immunology Inflammation Inflammatory bowel disease Interleukin 1 Interleukin 17 Interleukin 22 Interleukin-27 - immunology Interleukins - immunology Intestine Lymphocytes Lymphocytes - immunology Lymphoid cells Male Membrane Glycoproteins - immunology Mice Mice, Inbred C57BL Microorganisms Pathogens Peptides Physiology Protein composition Protein purification RAW 264.7 Cells Receptors Rodents Roles Small intestine Thymus gland Transcription factors |
| title | Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93 |
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