Therapeutic normal IgG intravenous immunoglobulin activates Wnt-β-catenin pathway in dendritic cells
Therapeutic normal IgG intravenous immunoglobulin (IVIG) is a well-established first-line immunotherapy for many autoimmune and inflammatory diseases. Though several mechanisms have been proposed for the anti-inflammatory actions of IVIG, associated signaling pathways are not well studied. As β-cate...
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| Veröffentlicht in: | Communications biology 2020-03, Vol.3 (1), p.96-96, Article 96 |
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| creator | Karnam, Anupama Rambabu, Naresh Das, Mrinmoy Bou-Jaoudeh, Melissa Delignat, Sandrine Käsermann, Fabian Lacroix-Desmazes, Sébastien Kaveri, Srini V. Bayry, Jagadeesh |
| description | Therapeutic normal IgG intravenous immunoglobulin (IVIG) is a well-established first-line immunotherapy for many autoimmune and inflammatory diseases. Though several mechanisms have been proposed for the anti-inflammatory actions of IVIG, associated signaling pathways are not well studied. As β-catenin, the central component of the canonical Wnt pathway, plays an important role in imparting tolerogenic properties to dendritic cells (DCs) and in reducing inflammation, we explored whether IVIG induces the β-catenin pathway to exert anti-inflammatory effects. We show that IVIG in an IgG-sialylation independent manner activates β-catenin in human DCs along with upregulation of Wnt5a secretion. Mechanistically, β-catenin activation by IVIG requires intact IgG and LRP5/6 co-receptors, but FcγRIIA and Syk are not implicated. Despite induction of β-catenin, this pathway is dispensable for anti-inflammatory actions of IVIG in vitro and for mediating the protection against experimental autoimmune encephalomyelitis in vivo in mice, and reciprocal regulation of effector Th17/Th1 and regulatory T cells.
Karnam et al. show that the β-catenin pathway is dispensable for the anti-inflammatory actions of intravenous immunoglobulin (IVIG) in human dendritic cells and in protecting against experimental autoimmune encephalomyelitis. This study implicates an unknown signaling pathway as a mediator of the anti-inflammatory effects of therapeutic IVIG. |
| doi_str_mv | 10.1038/s42003-020-0825-4 |
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Karnam et al. show that the β-catenin pathway is dispensable for the anti-inflammatory actions of intravenous immunoglobulin (IVIG) in human dendritic cells and in protecting against experimental autoimmune encephalomyelitis. This study implicates an unknown signaling pathway as a mediator of the anti-inflammatory effects of therapeutic IVIG.</description><identifier>ISSN: 2399-3642</identifier><identifier>EISSN: 2399-3642</identifier><identifier>DOI: 10.1038/s42003-020-0825-4</identifier><identifier>PMID: 32132640</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/21 ; 13/31 ; 13/89 ; 13/95 ; 38/39 ; 38/77 ; 38/90 ; 631/250/127 ; 631/250/2502 ; 631/250/251 ; 631/250/38 ; 64/60 ; 82/29 ; 96/109 ; Biology ; Biomedical and Life Sciences ; Dendritic cells ; Experimental allergic encephalomyelitis ; Helper cells ; Immunoglobulin G ; Immunoglobulins ; Immunology ; Immunoregulation ; Immunotherapy ; Inflammatory diseases ; Intravenous administration ; Life Sciences ; LRP5 protein ; Lymphocytes T ; Signal transduction ; Syk protein ; Wnt protein ; β-Catenin</subject><ispartof>Communications biology, 2020-03, Vol.3 (1), p.96-96, Article 96</ispartof><rights>The Author(s) 2020</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-bb61fa87ea9372b33167f5d60800dbb0cde23f1304f4612eb86c91923afdec4d3</citedby><cites>FETCH-LOGICAL-c507t-bb61fa87ea9372b33167f5d60800dbb0cde23f1304f4612eb86c91923afdec4d3</cites><orcidid>0000-0001-7649-3751 ; 0000-0002-9932-9548 ; 0000-0002-4255-9350 ; 0000-0003-0498-9808 ; 0000-0001-8770-186X ; 0000-0002-0837-4053 ; 0000-0001-5625-8447</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7055225/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7055225/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32132640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-02553449$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Karnam, Anupama</creatorcontrib><creatorcontrib>Rambabu, Naresh</creatorcontrib><creatorcontrib>Das, Mrinmoy</creatorcontrib><creatorcontrib>Bou-Jaoudeh, Melissa</creatorcontrib><creatorcontrib>Delignat, Sandrine</creatorcontrib><creatorcontrib>Käsermann, Fabian</creatorcontrib><creatorcontrib>Lacroix-Desmazes, Sébastien</creatorcontrib><creatorcontrib>Kaveri, Srini V.</creatorcontrib><creatorcontrib>Bayry, Jagadeesh</creatorcontrib><title>Therapeutic normal IgG intravenous immunoglobulin activates Wnt-β-catenin pathway in dendritic cells</title><title>Communications biology</title><addtitle>Commun Biol</addtitle><addtitle>Commun Biol</addtitle><description>Therapeutic normal IgG intravenous immunoglobulin (IVIG) is a well-established first-line immunotherapy for many autoimmune and inflammatory diseases. Though several mechanisms have been proposed for the anti-inflammatory actions of IVIG, associated signaling pathways are not well studied. As β-catenin, the central component of the canonical Wnt pathway, plays an important role in imparting tolerogenic properties to dendritic cells (DCs) and in reducing inflammation, we explored whether IVIG induces the β-catenin pathway to exert anti-inflammatory effects. We show that IVIG in an IgG-sialylation independent manner activates β-catenin in human DCs along with upregulation of Wnt5a secretion. Mechanistically, β-catenin activation by IVIG requires intact IgG and LRP5/6 co-receptors, but FcγRIIA and Syk are not implicated. Despite induction of β-catenin, this pathway is dispensable for anti-inflammatory actions of IVIG in vitro and for mediating the protection against experimental autoimmune encephalomyelitis in vivo in mice, and reciprocal regulation of effector Th17/Th1 and regulatory T cells.
Karnam et al. show that the β-catenin pathway is dispensable for the anti-inflammatory actions of intravenous immunoglobulin (IVIG) in human dendritic cells and in protecting against experimental autoimmune encephalomyelitis. This study implicates an unknown signaling pathway as a mediator of the anti-inflammatory effects of therapeutic IVIG.</description><subject>13/1</subject><subject>13/21</subject><subject>13/31</subject><subject>13/89</subject><subject>13/95</subject><subject>38/39</subject><subject>38/77</subject><subject>38/90</subject><subject>631/250/127</subject><subject>631/250/2502</subject><subject>631/250/251</subject><subject>631/250/38</subject><subject>64/60</subject><subject>82/29</subject><subject>96/109</subject><subject>Biology</subject><subject>Biomedical and Life Sciences</subject><subject>Dendritic cells</subject><subject>Experimental allergic encephalomyelitis</subject><subject>Helper cells</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulins</subject><subject>Immunology</subject><subject>Immunoregulation</subject><subject>Immunotherapy</subject><subject>Inflammatory diseases</subject><subject>Intravenous administration</subject><subject>Life Sciences</subject><subject>LRP5 protein</subject><subject>Lymphocytes T</subject><subject>Signal transduction</subject><subject>Syk protein</subject><subject>Wnt protein</subject><subject>β-Catenin</subject><issn>2399-3642</issn><issn>2399-3642</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kctu1TAQhi0EolXpA7BBkdiwwDC-5OINUlVBW-lIbIpYWo4zOcdVYh_s5FR9LR6EZ8JRSimV2Pii-eafy0_IawYfGIjmY5IcQFDgQKHhJZXPyDEXSlFRSf780fuInKZ0AwBMKVUJ-ZIcCc4EryQcE7zeYTR7nCdnCx_iaIbiantROD9Fc0Af5lS4cZx92A6hnQfnC2MndzATpuK7n-ivn9Tmj8-BvZl2t-Yu5xYd-i66RdPiMKRX5EVvhoSn9_cJ-fbl8_X5Jd18vbg6P9tQW0I90batWG-aGo0SNW-FYFXdl10FDUDXtmA75KJnAmQvK8axbSqrmOLC9B1a2YkT8mnV3c_tiJ3FZYpB76MbTbzTwTj9b8S7nd6Gg66hLDkvs8D7VWD3JO3ybKOdTxhHDbwshZTqwDL-7r5eDD9mTJMeXVomNh7z5jQXNWuysmwy-vYJehPm6PM2FqqWkuUjU2ylbAwpRewfmmCgF9v1antuAvRiu15y3jwe-iHjj8kZ4CuQcshvMf4t_X_V30aCugk</recordid><startdate>20200304</startdate><enddate>20200304</enddate><creator>Karnam, Anupama</creator><creator>Rambabu, Naresh</creator><creator>Das, Mrinmoy</creator><creator>Bou-Jaoudeh, Melissa</creator><creator>Delignat, Sandrine</creator><creator>Käsermann, Fabian</creator><creator>Lacroix-Desmazes, Sébastien</creator><creator>Kaveri, Srini V.</creator><creator>Bayry, Jagadeesh</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7XB</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7649-3751</orcidid><orcidid>https://orcid.org/0000-0002-9932-9548</orcidid><orcidid>https://orcid.org/0000-0002-4255-9350</orcidid><orcidid>https://orcid.org/0000-0003-0498-9808</orcidid><orcidid>https://orcid.org/0000-0001-8770-186X</orcidid><orcidid>https://orcid.org/0000-0002-0837-4053</orcidid><orcidid>https://orcid.org/0000-0001-5625-8447</orcidid></search><sort><creationdate>20200304</creationdate><title>Therapeutic normal IgG intravenous immunoglobulin activates Wnt-β-catenin pathway in dendritic cells</title><author>Karnam, Anupama ; Rambabu, Naresh ; Das, Mrinmoy ; Bou-Jaoudeh, Melissa ; Delignat, Sandrine ; Käsermann, Fabian ; Lacroix-Desmazes, Sébastien ; Kaveri, Srini V. ; Bayry, Jagadeesh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-bb61fa87ea9372b33167f5d60800dbb0cde23f1304f4612eb86c91923afdec4d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>13/1</topic><topic>13/21</topic><topic>13/31</topic><topic>13/89</topic><topic>13/95</topic><topic>38/39</topic><topic>38/77</topic><topic>38/90</topic><topic>631/250/127</topic><topic>631/250/2502</topic><topic>631/250/251</topic><topic>631/250/38</topic><topic>64/60</topic><topic>82/29</topic><topic>96/109</topic><topic>Biology</topic><topic>Biomedical and Life Sciences</topic><topic>Dendritic cells</topic><topic>Experimental allergic encephalomyelitis</topic><topic>Helper cells</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulins</topic><topic>Immunology</topic><topic>Immunoregulation</topic><topic>Immunotherapy</topic><topic>Inflammatory diseases</topic><topic>Intravenous administration</topic><topic>Life Sciences</topic><topic>LRP5 protein</topic><topic>Lymphocytes T</topic><topic>Signal transduction</topic><topic>Syk protein</topic><topic>Wnt protein</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Karnam, Anupama</creatorcontrib><creatorcontrib>Rambabu, Naresh</creatorcontrib><creatorcontrib>Das, Mrinmoy</creatorcontrib><creatorcontrib>Bou-Jaoudeh, Melissa</creatorcontrib><creatorcontrib>Delignat, Sandrine</creatorcontrib><creatorcontrib>Käsermann, Fabian</creatorcontrib><creatorcontrib>Lacroix-Desmazes, Sébastien</creatorcontrib><creatorcontrib>Kaveri, Srini V.</creatorcontrib><creatorcontrib>Bayry, Jagadeesh</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Communications biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Karnam, Anupama</au><au>Rambabu, Naresh</au><au>Das, Mrinmoy</au><au>Bou-Jaoudeh, Melissa</au><au>Delignat, Sandrine</au><au>Käsermann, Fabian</au><au>Lacroix-Desmazes, Sébastien</au><au>Kaveri, Srini V.</au><au>Bayry, Jagadeesh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic normal IgG intravenous immunoglobulin activates Wnt-β-catenin pathway in dendritic cells</atitle><jtitle>Communications biology</jtitle><stitle>Commun Biol</stitle><addtitle>Commun Biol</addtitle><date>2020-03-04</date><risdate>2020</risdate><volume>3</volume><issue>1</issue><spage>96</spage><epage>96</epage><pages>96-96</pages><artnum>96</artnum><issn>2399-3642</issn><eissn>2399-3642</eissn><abstract>Therapeutic normal IgG intravenous immunoglobulin (IVIG) is a well-established first-line immunotherapy for many autoimmune and inflammatory diseases. Though several mechanisms have been proposed for the anti-inflammatory actions of IVIG, associated signaling pathways are not well studied. As β-catenin, the central component of the canonical Wnt pathway, plays an important role in imparting tolerogenic properties to dendritic cells (DCs) and in reducing inflammation, we explored whether IVIG induces the β-catenin pathway to exert anti-inflammatory effects. We show that IVIG in an IgG-sialylation independent manner activates β-catenin in human DCs along with upregulation of Wnt5a secretion. Mechanistically, β-catenin activation by IVIG requires intact IgG and LRP5/6 co-receptors, but FcγRIIA and Syk are not implicated. Despite induction of β-catenin, this pathway is dispensable for anti-inflammatory actions of IVIG in vitro and for mediating the protection against experimental autoimmune encephalomyelitis in vivo in mice, and reciprocal regulation of effector Th17/Th1 and regulatory T cells.
Karnam et al. show that the β-catenin pathway is dispensable for the anti-inflammatory actions of intravenous immunoglobulin (IVIG) in human dendritic cells and in protecting against experimental autoimmune encephalomyelitis. This study implicates an unknown signaling pathway as a mediator of the anti-inflammatory effects of therapeutic IVIG.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32132640</pmid><doi>10.1038/s42003-020-0825-4</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-7649-3751</orcidid><orcidid>https://orcid.org/0000-0002-9932-9548</orcidid><orcidid>https://orcid.org/0000-0002-4255-9350</orcidid><orcidid>https://orcid.org/0000-0003-0498-9808</orcidid><orcidid>https://orcid.org/0000-0001-8770-186X</orcidid><orcidid>https://orcid.org/0000-0002-0837-4053</orcidid><orcidid>https://orcid.org/0000-0001-5625-8447</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/21 13/31 13/89 13/95 38/39 38/77 38/90 631/250/127 631/250/2502 631/250/251 631/250/38 64/60 82/29 96/109 Biology Biomedical and Life Sciences Dendritic cells Experimental allergic encephalomyelitis Helper cells Immunoglobulin G Immunoglobulins Immunology Immunoregulation Immunotherapy Inflammatory diseases Intravenous administration Life Sciences LRP5 protein Lymphocytes T Signal transduction Syk protein Wnt protein β-Catenin |
| title | Therapeutic normal IgG intravenous immunoglobulin activates Wnt-β-catenin pathway in dendritic cells |
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