A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis
Rheumatoid arthritis is characterized by progressive joint inflammation and affects ~1% of the human population. We noted single-nucleotide polymorphisms (SNPs) in the apoptotic cell–engulfment genes ELMO1, DOCK2 , and RAC1 linked to rheumatoid arthritis. As ELMO1 promotes cytoskeletal reorganizatio...
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| Veröffentlicht in: | Nature immunology 2019-02, Vol.20 (2), p.141-151 |
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| creator | Arandjelovic, Sanja Perry, Justin S. A. Lucas, Christopher D. Penberthy, Kristen K. Kim, Tae-Hyoun Zhou, Ming Rosen, Dorian A Chuang, Tzu-Ying Bettina, Alexandra M. Shankman, Laura S. Cohen, Amanda H. Gaultier, Alban Conrads, Thomas P. Kim, Minsoo Elliott, Michael R. Ravichandran, Kodi S. |
| description | Rheumatoid arthritis is characterized by progressive joint inflammation and affects ~1% of the human population. We noted single-nucleotide polymorphisms (SNPs) in the apoptotic cell–engulfment genes
ELMO1, DOCK2
, and
RAC1
linked to rheumatoid arthritis. As ELMO1 promotes cytoskeletal reorganization during engulfment, we hypothesized that ELMO1 loss would worsen inflammatory arthritis. Surprisingly,
Elmo1
-deficient mice showed reduced joint inflammation in acute and chronic arthritis models. Genetic and cell-biology studies revealed that ELMO1 associates with receptors linked to neutrophil function in arthritis and regulates activation and early neutrophil recruitment to the joints, without general inhibition of inflammatory responses. Further, neutrophils from the peripheral blood of human donors that carry the SNP in
ELMO1
associated with arthritis display increased migratory capacity, whereas
ELMO1
knockdown reduces human neutrophil migration to chemokines linked to arthritis. These data identify ‘noncanonical’ roles for ELMO1 as an important cytoplasmic regulator of specific neutrophil receptors and promoter of arthritis.
ELMO1 is a protein centrally involved in controlling the engulfment of apoptotic cells. Ravichandran and colleagues demonstrate a noncanonical role for ELMO1 in the promotion of neutrophil migration and inflammatory arthritis. |
| doi_str_mv | 10.1038/s41590-018-0293-x |
| format | Article |
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ELMO1, DOCK2
, and
RAC1
linked to rheumatoid arthritis. As ELMO1 promotes cytoskeletal reorganization during engulfment, we hypothesized that ELMO1 loss would worsen inflammatory arthritis. Surprisingly,
Elmo1
-deficient mice showed reduced joint inflammation in acute and chronic arthritis models. Genetic and cell-biology studies revealed that ELMO1 associates with receptors linked to neutrophil function in arthritis and regulates activation and early neutrophil recruitment to the joints, without general inhibition of inflammatory responses. Further, neutrophils from the peripheral blood of human donors that carry the SNP in
ELMO1
associated with arthritis display increased migratory capacity, whereas
ELMO1
knockdown reduces human neutrophil migration to chemokines linked to arthritis. These data identify ‘noncanonical’ roles for ELMO1 as an important cytoplasmic regulator of specific neutrophil receptors and promoter of arthritis.
ELMO1 is a protein centrally involved in controlling the engulfment of apoptotic cells. Ravichandran and colleagues demonstrate a noncanonical role for ELMO1 in the promotion of neutrophil migration and inflammatory arthritis.</description><identifier>ISSN: 1529-2908</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/s41590-018-0293-x</identifier><identifier>PMID: 30643265</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/250 ; 631/337 ; 631/80 ; 692/699/249 ; Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - immunology ; Animal models ; Animals ; Apoptosis ; Apoptosis - immunology ; Arthritis ; Arthritis, Experimental - diagnosis ; Arthritis, Experimental - genetics ; Arthritis, Experimental - immunology ; Arthritis, Experimental - pathology ; Arthritis, Rheumatoid - diagnosis ; Arthritis, Rheumatoid - genetics ; Arthritis, Rheumatoid - immunology ; Arthritis, Rheumatoid - pathology ; Biomedical and Life Sciences ; Biomedicine ; Cell activation ; Cell culture ; Chemokines ; Chemotaxis - genetics ; Chemotaxis - immunology ; Collagen - immunology ; Complement C5a - immunology ; Complement C5a - metabolism ; Cytoplasm - immunology ; Cytoplasm - metabolism ; Cytoskeleton ; Disease Models, Animal ; Female ; Gene Expression Profiling ; Genes ; Genetic aspects ; Genetic polymorphisms ; Healthy Volunteers ; Human migration ; Human populations ; Humans ; Immunology ; Infectious Diseases ; Inflammation ; Intravital Microscopy ; Joint diseases ; Joints - cytology ; Joints - immunology ; Leukocyte migration ; Leukocytes (neutrophilic) ; Leukotriene B4 - immunology ; Leukotriene B4 - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils ; Neutrophils - immunology ; Neutrophils - metabolism ; Peripheral blood ; Polymorphism, Single Nucleotide ; Promoters (Genetics) ; Proteomics ; Rac1 protein ; Receptor mechanisms ; Rheumatoid arthritis ; Rheumatoid factor ; Severity of Illness Index ; Signal Transduction - immunology ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Time-Lapse Imaging</subject><ispartof>Nature immunology, 2019-02, Vol.20 (2), p.141-151</ispartof><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. 2019</rights><rights>COPYRIGHT 2019 Nature Publishing Group</rights><rights>2019© The Author(s), under exclusive licence to Springer Nature America, Inc. 2019</rights><rights>The Author(s), under exclusive licence to Springer Nature America, Inc. 2019.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c544t-e0ec80c027e93dcd95db7abc0c6bd3159125f71d5ca2a543a64e450f0680859f3</citedby><cites>FETCH-LOGICAL-c544t-e0ec80c027e93dcd95db7abc0c6bd3159125f71d5ca2a543a64e450f0680859f3</cites><orcidid>0000-0003-3178-0524 ; 0000-0002-4175-6053 ; 0000-0003-1113-1965 ; 0000-0003-3511-238X ; 0000-0001-9049-1410</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/s41590-018-0293-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41590-018-0293-x$$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/30643265$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arandjelovic, Sanja</creatorcontrib><creatorcontrib>Perry, Justin S. A.</creatorcontrib><creatorcontrib>Lucas, Christopher D.</creatorcontrib><creatorcontrib>Penberthy, Kristen K.</creatorcontrib><creatorcontrib>Kim, Tae-Hyoun</creatorcontrib><creatorcontrib>Zhou, Ming</creatorcontrib><creatorcontrib>Rosen, Dorian A</creatorcontrib><creatorcontrib>Chuang, Tzu-Ying</creatorcontrib><creatorcontrib>Bettina, Alexandra M.</creatorcontrib><creatorcontrib>Shankman, Laura S.</creatorcontrib><creatorcontrib>Cohen, Amanda H.</creatorcontrib><creatorcontrib>Gaultier, Alban</creatorcontrib><creatorcontrib>Conrads, Thomas P.</creatorcontrib><creatorcontrib>Kim, Minsoo</creatorcontrib><creatorcontrib>Elliott, Michael R.</creatorcontrib><creatorcontrib>Ravichandran, Kodi S.</creatorcontrib><title>A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><addtitle>Nat Immunol</addtitle><description>Rheumatoid arthritis is characterized by progressive joint inflammation and affects ~1% of the human population. We noted single-nucleotide polymorphisms (SNPs) in the apoptotic cell–engulfment genes
ELMO1, DOCK2
, and
RAC1
linked to rheumatoid arthritis. As ELMO1 promotes cytoskeletal reorganization during engulfment, we hypothesized that ELMO1 loss would worsen inflammatory arthritis. Surprisingly,
Elmo1
-deficient mice showed reduced joint inflammation in acute and chronic arthritis models. Genetic and cell-biology studies revealed that ELMO1 associates with receptors linked to neutrophil function in arthritis and regulates activation and early neutrophil recruitment to the joints, without general inhibition of inflammatory responses. Further, neutrophils from the peripheral blood of human donors that carry the SNP in
ELMO1
associated with arthritis display increased migratory capacity, whereas
ELMO1
knockdown reduces human neutrophil migration to chemokines linked to arthritis. These data identify ‘noncanonical’ roles for ELMO1 as an important cytoplasmic regulator of specific neutrophil receptors and promoter of arthritis.
ELMO1 is a protein centrally involved in controlling the engulfment of apoptotic cells. Ravichandran and colleagues demonstrate a noncanonical role for ELMO1 in the promotion of neutrophil migration and inflammatory arthritis.</description><subject>631/250</subject><subject>631/337</subject><subject>631/80</subject><subject>692/699/249</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - immunology</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - immunology</subject><subject>Arthritis</subject><subject>Arthritis, Experimental - diagnosis</subject><subject>Arthritis, Experimental - genetics</subject><subject>Arthritis, Experimental - immunology</subject><subject>Arthritis, Experimental - pathology</subject><subject>Arthritis, Rheumatoid - diagnosis</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Arthritis, Rheumatoid - immunology</subject><subject>Arthritis, Rheumatoid - pathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell activation</subject><subject>Cell culture</subject><subject>Chemokines</subject><subject>Chemotaxis - genetics</subject><subject>Chemotaxis - immunology</subject><subject>Collagen - immunology</subject><subject>Complement C5a - immunology</subject><subject>Complement C5a - metabolism</subject><subject>Cytoplasm - immunology</subject><subject>Cytoplasm - metabolism</subject><subject>Cytoskeleton</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Gene Expression Profiling</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Healthy Volunteers</subject><subject>Human migration</subject><subject>Human populations</subject><subject>Humans</subject><subject>Immunology</subject><subject>Infectious Diseases</subject><subject>Inflammation</subject><subject>Intravital Microscopy</subject><subject>Joint diseases</subject><subject>Joints - cytology</subject><subject>Joints - immunology</subject><subject>Leukocyte migration</subject><subject>Leukocytes (neutrophilic)</subject><subject>Leukotriene B4 - immunology</subject><subject>Leukotriene B4 - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neutrophils</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - metabolism</subject><subject>Peripheral blood</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Promoters (Genetics)</subject><subject>Proteomics</subject><subject>Rac1 protein</subject><subject>Receptor mechanisms</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatoid factor</subject><subject>Severity of Illness Index</subject><subject>Signal Transduction - immunology</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Time-Lapse Imaging</subject><issn>1529-2908</issn><issn>1529-2916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kstq3DAUhk1paC7tA3RTBN00CydHV9vLIaRtYEogbddCIx97HGxpKskweftqmDRhShsEktD5_nMRf1G8p3BBgdeXUVDZQAm0LoE1vNy-Kk6oZE3JGqpeP92hPi5OY7wHoKJS4k1xzEEJzpQ8KXBBnHfW5G2wZiTBj0g6H0haI0HXz2M3oUukR4fkevntlpLBEYdzCn6zHsaYQZPIJvjJJ4w52I1mmkzy4YGYkNZhSEN8Wxx1Zoz47vE8K35-vv5x9bVc3n65uVosSyuFSCUC2hossAob3tq2ke2qMisLVq1anmelTHYVbaU1zEjBjRIoJHSgaqhl0_Gz4tM-b-7n14wx6WmIFsfROPRz1IxWDZd1XfGMfvwLvfdzcLk7zUQlQXCVK7xEUdWwWihQz1RvRtT5C3wKxu5K64WsmALOKc3UxT-ovFqcBusddkN-PxCcHwgyk3CbejPHqG--3x2ydM_a4GMM2OlNGCYTHjQFvTOL3ptFZ7PonVn0Nms-PA43ryZsnxR_3JEBtgdiDrkew_P0_8_6G69uxyw</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Arandjelovic, Sanja</creator><creator>Perry, Justin S. A.</creator><creator>Lucas, Christopher D.</creator><creator>Penberthy, Kristen K.</creator><creator>Kim, Tae-Hyoun</creator><creator>Zhou, Ming</creator><creator>Rosen, Dorian A</creator><creator>Chuang, Tzu-Ying</creator><creator>Bettina, Alexandra M.</creator><creator>Shankman, Laura S.</creator><creator>Cohen, Amanda H.</creator><creator>Gaultier, Alban</creator><creator>Conrads, Thomas P.</creator><creator>Kim, Minsoo</creator><creator>Elliott, Michael R.</creator><creator>Ravichandran, Kodi S.</creator><general>Nature Publishing Group US</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3178-0524</orcidid><orcidid>https://orcid.org/0000-0002-4175-6053</orcidid><orcidid>https://orcid.org/0000-0003-1113-1965</orcidid><orcidid>https://orcid.org/0000-0003-3511-238X</orcidid><orcidid>https://orcid.org/0000-0001-9049-1410</orcidid></search><sort><creationdate>20190201</creationdate><title>A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis</title><author>Arandjelovic, Sanja ; Perry, Justin S. A. ; Lucas, Christopher D. ; Penberthy, Kristen K. ; Kim, Tae-Hyoun ; Zhou, Ming ; Rosen, Dorian A ; Chuang, Tzu-Ying ; Bettina, Alexandra M. ; Shankman, Laura S. ; Cohen, Amanda H. ; Gaultier, Alban ; Conrads, Thomas P. ; Kim, Minsoo ; Elliott, Michael R. ; Ravichandran, Kodi S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c544t-e0ec80c027e93dcd95db7abc0c6bd3159125f71d5ca2a543a64e450f0680859f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>631/250</topic><topic>631/337</topic><topic>631/80</topic><topic>692/699/249</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - immunology</topic><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - immunology</topic><topic>Arthritis</topic><topic>Arthritis, Experimental - diagnosis</topic><topic>Arthritis, Experimental - genetics</topic><topic>Arthritis, Experimental - immunology</topic><topic>Arthritis, Experimental - pathology</topic><topic>Arthritis, Rheumatoid - diagnosis</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Arthritis, Rheumatoid - immunology</topic><topic>Arthritis, Rheumatoid - pathology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell activation</topic><topic>Cell culture</topic><topic>Chemokines</topic><topic>Chemotaxis - genetics</topic><topic>Chemotaxis - immunology</topic><topic>Collagen - immunology</topic><topic>Complement C5a - immunology</topic><topic>Complement C5a - metabolism</topic><topic>Cytoplasm - immunology</topic><topic>Cytoplasm - metabolism</topic><topic>Cytoskeleton</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Gene Expression Profiling</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Healthy Volunteers</topic><topic>Human migration</topic><topic>Human populations</topic><topic>Humans</topic><topic>Immunology</topic><topic>Infectious Diseases</topic><topic>Inflammation</topic><topic>Intravital Microscopy</topic><topic>Joint diseases</topic><topic>Joints - cytology</topic><topic>Joints - immunology</topic><topic>Leukocyte migration</topic><topic>Leukocytes (neutrophilic)</topic><topic>Leukotriene B4 - immunology</topic><topic>Leukotriene B4 - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Neutrophils</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - metabolism</topic><topic>Peripheral blood</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Promoters (Genetics)</topic><topic>Proteomics</topic><topic>Rac1 protein</topic><topic>Receptor mechanisms</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatoid factor</topic><topic>Severity of Illness Index</topic><topic>Signal Transduction - immunology</topic><topic>Single nucleotide polymorphisms</topic><topic>Single-nucleotide polymorphism</topic><topic>Time-Lapse Imaging</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arandjelovic, Sanja</creatorcontrib><creatorcontrib>Perry, Justin S. 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A.</au><au>Lucas, Christopher D.</au><au>Penberthy, Kristen K.</au><au>Kim, Tae-Hyoun</au><au>Zhou, Ming</au><au>Rosen, Dorian A</au><au>Chuang, Tzu-Ying</au><au>Bettina, Alexandra M.</au><au>Shankman, Laura S.</au><au>Cohen, Amanda H.</au><au>Gaultier, Alban</au><au>Conrads, Thomas P.</au><au>Kim, Minsoo</au><au>Elliott, Michael R.</au><au>Ravichandran, Kodi S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis</atitle><jtitle>Nature immunology</jtitle><stitle>Nat Immunol</stitle><addtitle>Nat Immunol</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>20</volume><issue>2</issue><spage>141</spage><epage>151</epage><pages>141-151</pages><issn>1529-2908</issn><eissn>1529-2916</eissn><abstract>Rheumatoid arthritis is characterized by progressive joint inflammation and affects ~1% of the human population. We noted single-nucleotide polymorphisms (SNPs) in the apoptotic cell–engulfment genes
ELMO1, DOCK2
, and
RAC1
linked to rheumatoid arthritis. As ELMO1 promotes cytoskeletal reorganization during engulfment, we hypothesized that ELMO1 loss would worsen inflammatory arthritis. Surprisingly,
Elmo1
-deficient mice showed reduced joint inflammation in acute and chronic arthritis models. Genetic and cell-biology studies revealed that ELMO1 associates with receptors linked to neutrophil function in arthritis and regulates activation and early neutrophil recruitment to the joints, without general inhibition of inflammatory responses. Further, neutrophils from the peripheral blood of human donors that carry the SNP in
ELMO1
associated with arthritis display increased migratory capacity, whereas
ELMO1
knockdown reduces human neutrophil migration to chemokines linked to arthritis. These data identify ‘noncanonical’ roles for ELMO1 as an important cytoplasmic regulator of specific neutrophil receptors and promoter of arthritis.
ELMO1 is a protein centrally involved in controlling the engulfment of apoptotic cells. Ravichandran and colleagues demonstrate a noncanonical role for ELMO1 in the promotion of neutrophil migration and inflammatory arthritis.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>30643265</pmid><doi>10.1038/s41590-018-0293-x</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-3178-0524</orcidid><orcidid>https://orcid.org/0000-0002-4175-6053</orcidid><orcidid>https://orcid.org/0000-0003-1113-1965</orcidid><orcidid>https://orcid.org/0000-0003-3511-238X</orcidid><orcidid>https://orcid.org/0000-0001-9049-1410</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1529-2908 |
| ispartof | Nature immunology, 2019-02, Vol.20 (2), p.141-151 |
| issn | 1529-2908 1529-2916 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2179358873 |
| source | MEDLINE; SpringerLink Journals; Nature Journals Online |
| subjects | 631/250 631/337 631/80 692/699/249 Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - immunology Animal models Animals Apoptosis Apoptosis - immunology Arthritis Arthritis, Experimental - diagnosis Arthritis, Experimental - genetics Arthritis, Experimental - immunology Arthritis, Experimental - pathology Arthritis, Rheumatoid - diagnosis Arthritis, Rheumatoid - genetics Arthritis, Rheumatoid - immunology Arthritis, Rheumatoid - pathology Biomedical and Life Sciences Biomedicine Cell activation Cell culture Chemokines Chemotaxis - genetics Chemotaxis - immunology Collagen - immunology Complement C5a - immunology Complement C5a - metabolism Cytoplasm - immunology Cytoplasm - metabolism Cytoskeleton Disease Models, Animal Female Gene Expression Profiling Genes Genetic aspects Genetic polymorphisms Healthy Volunteers Human migration Human populations Humans Immunology Infectious Diseases Inflammation Intravital Microscopy Joint diseases Joints - cytology Joints - immunology Leukocyte migration Leukocytes (neutrophilic) Leukotriene B4 - immunology Leukotriene B4 - metabolism Male Mice Mice, Inbred C57BL Mice, Knockout Neutrophils Neutrophils - immunology Neutrophils - metabolism Peripheral blood Polymorphism, Single Nucleotide Promoters (Genetics) Proteomics Rac1 protein Receptor mechanisms Rheumatoid arthritis Rheumatoid factor Severity of Illness Index Signal Transduction - immunology Single nucleotide polymorphisms Single-nucleotide polymorphism Time-Lapse Imaging |
| title | A noncanonical role for the engulfment gene ELMO1 in neutrophils that promotes inflammatory arthritis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T05%3A30%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20noncanonical%20role%20for%20the%20engulfment%20gene%20ELMO1%20in%20neutrophils%20that%20promotes%20inflammatory%20arthritis&rft.jtitle=Nature%20immunology&rft.au=Arandjelovic,%20Sanja&rft.date=2019-02-01&rft.volume=20&rft.issue=2&rft.spage=141&rft.epage=151&rft.pages=141-151&rft.issn=1529-2908&rft.eissn=1529-2916&rft_id=info:doi/10.1038/s41590-018-0293-x&rft_dat=%3Cgale_proqu%3EA572603311%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2169284606&rft_id=info:pmid/30643265&rft_galeid=A572603311&rfr_iscdi=true |