IgG Immunocomplexes Drive the Differentiation of a Novel Subset of Osteoclasts Independent of RANKL and Inflammatory Cytokines
ABSTRACT Potentiation of receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis by IgG immunocomplexes (ICs) is generally considered an important pathway leading to cartilage and bone destruction in rheumatoid arthritis (RA). However, whether IgG ICs possess pro‐osteoclastogenic poten...
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| Veröffentlicht in: | Journal of bone and mineral research 2021-06, Vol.36 (6), p.1174-1188 |
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| container_title | Journal of bone and mineral research |
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| creator | Zeng, Ke‐Qin Gong, Fang‐Yuan Pan, Xiao‐Hua Miao, Jie Gong, Zheng Wang, Jun Zhong, Qiao Dai, Xia‐Qiu Gao, Xiao‐Ming |
| description | ABSTRACT
Potentiation of receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis by IgG immunocomplexes (ICs) is generally considered an important pathway leading to cartilage and bone destruction in rheumatoid arthritis (RA). However, whether IgG ICs possess pro‐osteoclastogenic potential independent of RANKL and inflammatory cytokines is unclear. Here we demonstrate that by fully cross‐linking human FcγRIIa (hFcγRIIa) or co‐ligating hFcγRIIa and TLR4, IgG ICs alone could drive the differentiation of human blood monocytes into nuclear factor of activated T cells cytoplasmic 1 (NFATc1‐negative nonclassical osteoclasts (NOCs). Surprisingly, IgG ICs could also overrule RANKL‐induced classical osteoclast (COC) differentiation in vitro. In mouse model of collagen‐induced arthritis, hFcγRIIa‐transgenic, but not nontransgenic control, mice suffered from cartilage/bone destruction accompanied by the presence of NFATc1− NOCs lining the eroded cartilage surface in affected joints. Our results not only identify a novel subset of IC‐induced NOCs but also provide a possible explanation for the uncoupling of FcγR‐mediated cartilage destruction from RANKL‐related bone erosion in autoinflammatory arthritis. © 2021 American Society for Bone and Mineral Research (ASBMR).. |
| doi_str_mv | 10.1002/jbmr.4281 |
| format | Article |
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Potentiation of receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis by IgG immunocomplexes (ICs) is generally considered an important pathway leading to cartilage and bone destruction in rheumatoid arthritis (RA). However, whether IgG ICs possess pro‐osteoclastogenic potential independent of RANKL and inflammatory cytokines is unclear. Here we demonstrate that by fully cross‐linking human FcγRIIa (hFcγRIIa) or co‐ligating hFcγRIIa and TLR4, IgG ICs alone could drive the differentiation of human blood monocytes into nuclear factor of activated T cells cytoplasmic 1 (NFATc1‐negative nonclassical osteoclasts (NOCs). Surprisingly, IgG ICs could also overrule RANKL‐induced classical osteoclast (COC) differentiation in vitro. In mouse model of collagen‐induced arthritis, hFcγRIIa‐transgenic, but not nontransgenic control, mice suffered from cartilage/bone destruction accompanied by the presence of NFATc1− NOCs lining the eroded cartilage surface in affected joints. Our results not only identify a novel subset of IC‐induced NOCs but also provide a possible explanation for the uncoupling of FcγR‐mediated cartilage destruction from RANKL‐related bone erosion in autoinflammatory arthritis. © 2021 American Society for Bone and Mineral Research (ASBMR)..</description><identifier>ISSN: 0884-0431</identifier><identifier>EISSN: 1523-4681</identifier><identifier>DOI: 10.1002/jbmr.4281</identifier><identifier>PMID: 33651383</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>Arthritis ; BONE EROSION ; Cartilage ; Collagen ; Cytokines ; FCGAMMA RECEPTOR IIa ; IMMUNOCOMPLEX ; Immunoglobulin G ; Inflammation ; Joint diseases ; Monocytes ; NF-AT protein ; NON‐CLASSIC OSTEOCLAST ; Osteoclastogenesis ; Osteoclasts ; RHEUMATOID ARTHRITIS ; TLR4 protein ; Toll-like receptors ; TRANCE protein ; Transcription factors</subject><ispartof>Journal of bone and mineral research, 2021-06, Vol.36 (6), p.1174-1188</ispartof><rights>2021 American Society for Bone and Mineral Research (ASBMR).</rights><rights>2021 American Society for Bone and Mineral Research</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4191-ea94acedd152d2785cb675986153e9687715d37c4c6fef073efbcf6cde814dfc3</citedby><cites>FETCH-LOGICAL-c4191-ea94acedd152d2785cb675986153e9687715d37c4c6fef073efbcf6cde814dfc3</cites><orcidid>0000-0002-8968-3252</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbmr.4281$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbmr.4281$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33651383$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zeng, Ke‐Qin</creatorcontrib><creatorcontrib>Gong, Fang‐Yuan</creatorcontrib><creatorcontrib>Pan, Xiao‐Hua</creatorcontrib><creatorcontrib>Miao, Jie</creatorcontrib><creatorcontrib>Gong, Zheng</creatorcontrib><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Zhong, Qiao</creatorcontrib><creatorcontrib>Dai, Xia‐Qiu</creatorcontrib><creatorcontrib>Gao, Xiao‐Ming</creatorcontrib><title>IgG Immunocomplexes Drive the Differentiation of a Novel Subset of Osteoclasts Independent of RANKL and Inflammatory Cytokines</title><title>Journal of bone and mineral research</title><addtitle>J Bone Miner Res</addtitle><description>ABSTRACT
Potentiation of receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis by IgG immunocomplexes (ICs) is generally considered an important pathway leading to cartilage and bone destruction in rheumatoid arthritis (RA). However, whether IgG ICs possess pro‐osteoclastogenic potential independent of RANKL and inflammatory cytokines is unclear. Here we demonstrate that by fully cross‐linking human FcγRIIa (hFcγRIIa) or co‐ligating hFcγRIIa and TLR4, IgG ICs alone could drive the differentiation of human blood monocytes into nuclear factor of activated T cells cytoplasmic 1 (NFATc1‐negative nonclassical osteoclasts (NOCs). Surprisingly, IgG ICs could also overrule RANKL‐induced classical osteoclast (COC) differentiation in vitro. In mouse model of collagen‐induced arthritis, hFcγRIIa‐transgenic, but not nontransgenic control, mice suffered from cartilage/bone destruction accompanied by the presence of NFATc1− NOCs lining the eroded cartilage surface in affected joints. Our results not only identify a novel subset of IC‐induced NOCs but also provide a possible explanation for the uncoupling of FcγR‐mediated cartilage destruction from RANKL‐related bone erosion in autoinflammatory arthritis. © 2021 American Society for Bone and Mineral Research (ASBMR)..</description><subject>Arthritis</subject><subject>BONE EROSION</subject><subject>Cartilage</subject><subject>Collagen</subject><subject>Cytokines</subject><subject>FCGAMMA RECEPTOR IIa</subject><subject>IMMUNOCOMPLEX</subject><subject>Immunoglobulin G</subject><subject>Inflammation</subject><subject>Joint diseases</subject><subject>Monocytes</subject><subject>NF-AT protein</subject><subject>NON‐CLASSIC OSTEOCLAST</subject><subject>Osteoclastogenesis</subject><subject>Osteoclasts</subject><subject>RHEUMATOID ARTHRITIS</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>TRANCE protein</subject><subject>Transcription factors</subject><issn>0884-0431</issn><issn>1523-4681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp1kU9v1DAQxS0EokvhwBdAlrjAIa0d_4lzLFsoC0srFThbjj2GLIm92E5hL3x2st3CAYnLG2neT08zegg9peSEElKfbroxnfBa0XtoQUXNKi4VvY8WRCleEc7oEXqU84YQIoWUD9ERY1JQptgC_Vp9ucCrcZxCtHHcDvATMj5P_Q3g8hXwee89JAilN6WPAUePDb6MNzDgj1OXoew3V7lAtIPJJeNVcLCFWcKtdX12-X6NTXCz4QczjqbEtMPLXYnf-gD5MXrgzZDhyd08Rp_fvP60fFutry5Wy7N1ZTltaQWm5caCc_N3rm6UsJ1sRKskFQxaqZqGCscay6304EnDwHfWS-tAUe68ZcfoxSF3m-L3CXLRY58tDIMJEKesa94KTmahM_r8H3QTpxTm63QtOK1F0zA2Uy8PlE0x5wReb1M_mrTTlOh9KXpfit6XMrPP7hKnbgT3l_zTwgycHoAf_QC7_yfpd68-XN9G_gbeiZeg</recordid><startdate>202106</startdate><enddate>202106</enddate><creator>Zeng, Ke‐Qin</creator><creator>Gong, Fang‐Yuan</creator><creator>Pan, Xiao‐Hua</creator><creator>Miao, Jie</creator><creator>Gong, Zheng</creator><creator>Wang, Jun</creator><creator>Zhong, Qiao</creator><creator>Dai, Xia‐Qiu</creator><creator>Gao, Xiao‐Ming</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TS</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8968-3252</orcidid></search><sort><creationdate>202106</creationdate><title>IgG Immunocomplexes Drive the Differentiation of a Novel Subset of Osteoclasts Independent of RANKL and Inflammatory Cytokines</title><author>Zeng, Ke‐Qin ; Gong, Fang‐Yuan ; Pan, Xiao‐Hua ; Miao, Jie ; Gong, Zheng ; Wang, Jun ; Zhong, Qiao ; Dai, Xia‐Qiu ; Gao, Xiao‐Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4191-ea94acedd152d2785cb675986153e9687715d37c4c6fef073efbcf6cde814dfc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Arthritis</topic><topic>BONE EROSION</topic><topic>Cartilage</topic><topic>Collagen</topic><topic>Cytokines</topic><topic>FCGAMMA RECEPTOR IIa</topic><topic>IMMUNOCOMPLEX</topic><topic>Immunoglobulin G</topic><topic>Inflammation</topic><topic>Joint diseases</topic><topic>Monocytes</topic><topic>NF-AT protein</topic><topic>NON‐CLASSIC OSTEOCLAST</topic><topic>Osteoclastogenesis</topic><topic>Osteoclasts</topic><topic>RHEUMATOID ARTHRITIS</topic><topic>TLR4 protein</topic><topic>Toll-like receptors</topic><topic>TRANCE protein</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Ke‐Qin</creatorcontrib><creatorcontrib>Gong, Fang‐Yuan</creatorcontrib><creatorcontrib>Pan, Xiao‐Hua</creatorcontrib><creatorcontrib>Miao, Jie</creatorcontrib><creatorcontrib>Gong, Zheng</creatorcontrib><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Zhong, Qiao</creatorcontrib><creatorcontrib>Dai, Xia‐Qiu</creatorcontrib><creatorcontrib>Gao, Xiao‐Ming</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Physical Education Index</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of bone and mineral research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Ke‐Qin</au><au>Gong, Fang‐Yuan</au><au>Pan, Xiao‐Hua</au><au>Miao, Jie</au><au>Gong, Zheng</au><au>Wang, Jun</au><au>Zhong, Qiao</au><au>Dai, Xia‐Qiu</au><au>Gao, Xiao‐Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IgG Immunocomplexes Drive the Differentiation of a Novel Subset of Osteoclasts Independent of RANKL and Inflammatory Cytokines</atitle><jtitle>Journal of bone and mineral research</jtitle><addtitle>J Bone Miner Res</addtitle><date>2021-06</date><risdate>2021</risdate><volume>36</volume><issue>6</issue><spage>1174</spage><epage>1188</epage><pages>1174-1188</pages><issn>0884-0431</issn><eissn>1523-4681</eissn><abstract>ABSTRACT
Potentiation of receptor activator of NF‐κB ligand (RANKL)‐induced osteoclastogenesis by IgG immunocomplexes (ICs) is generally considered an important pathway leading to cartilage and bone destruction in rheumatoid arthritis (RA). However, whether IgG ICs possess pro‐osteoclastogenic potential independent of RANKL and inflammatory cytokines is unclear. Here we demonstrate that by fully cross‐linking human FcγRIIa (hFcγRIIa) or co‐ligating hFcγRIIa and TLR4, IgG ICs alone could drive the differentiation of human blood monocytes into nuclear factor of activated T cells cytoplasmic 1 (NFATc1‐negative nonclassical osteoclasts (NOCs). Surprisingly, IgG ICs could also overrule RANKL‐induced classical osteoclast (COC) differentiation in vitro. In mouse model of collagen‐induced arthritis, hFcγRIIa‐transgenic, but not nontransgenic control, mice suffered from cartilage/bone destruction accompanied by the presence of NFATc1− NOCs lining the eroded cartilage surface in affected joints. Our results not only identify a novel subset of IC‐induced NOCs but also provide a possible explanation for the uncoupling of FcγR‐mediated cartilage destruction from RANKL‐related bone erosion in autoinflammatory arthritis. © 2021 American Society for Bone and Mineral Research (ASBMR)..</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>33651383</pmid><doi>10.1002/jbmr.4281</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-8968-3252</orcidid></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Arthritis BONE EROSION Cartilage Collagen Cytokines FCGAMMA RECEPTOR IIa IMMUNOCOMPLEX Immunoglobulin G Inflammation Joint diseases Monocytes NF-AT protein NON‐CLASSIC OSTEOCLAST Osteoclastogenesis Osteoclasts RHEUMATOID ARTHRITIS TLR4 protein Toll-like receptors TRANCE protein Transcription factors |
| title | IgG Immunocomplexes Drive the Differentiation of a Novel Subset of Osteoclasts Independent of RANKL and Inflammatory Cytokines |
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