IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathway
Abstract Objectives Tumor necrosis factor‐α (TNF‐α) plays a pivotal role in bone damage associated with inflammatory arthritis such as rheumatoid arthritis (RA). Both systemic lupus erythematosus (SLE) and rheumatoid arthritis exhibit clinical manifestations of inflammatory arthritis, yet the joint...
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| Format: | Article |
| Language: | English |
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Wiley
2025-01-01
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| Series: | Clinical & Translational Immunology |
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| Online Access: | https://doi.org/10.1002/cti2.70034 |
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| author | Haifeng Yin Yao Teng Guo‐Min Deng |
| author_facet | Haifeng Yin Yao Teng Guo‐Min Deng |
| author_sort | Haifeng Yin |
| collection | DOAJ |
| description | Abstract Objectives Tumor necrosis factor‐α (TNF‐α) plays a pivotal role in bone damage associated with inflammatory arthritis such as rheumatoid arthritis (RA). Both systemic lupus erythematosus (SLE) and rheumatoid arthritis exhibit clinical manifestations of inflammatory arthritis, yet the joint bone damage in RA is more severe than that in SLE. The reasons for this differential manifestation remain unclear. This study aimed to determine the role of IgG antibodies in TNF‐α‐induced osteoclastogenesis. Methods We conducted cellular experiments to ascertain whether IgG affects TNF‐α‐induced osteoclastogenesis and validate the role of IgG in TNF‐α‐induced cartilage destruction in mouse models of arthritis through animal studies. Results We found that IgG promoted TNF‐α‐induced osteoclastogenesis by upregulating the expression of tumor necrosis factor receptor 1 (TNFR1) and enhancing the downstream nuclear factor‐kappaB (NF‐κB) signalling pathway. In the TNF‐α‐induced arthritis mouse model, IgG further exacerbated the destruction of articular cartilage. Conclusion Our findings clarified that IgG aggravated TNF‐α‐mediated osteoclastogenesis, further elucidating the mechanistic basis for the divergent manifestations of joint bone damage in SLE and RA. |
| format | Article |
| id | doaj-art-b3b385423e744e4e8d605eb7b1bcf2b4 |
| institution | DOAJ |
| issn | 2050-0068 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Clinical & Translational Immunology |
| spelling | doaj-art-b3b385423e744e4e8d605eb7b1bcf2b42025-08-20T03:12:49ZengWileyClinical & Translational Immunology2050-00682025-01-01145n/an/a10.1002/cti2.70034IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathwayHaifeng Yin0Yao Teng1Guo‐Min Deng2Department of Rheumatology and Immunology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan ChinaDepartment of Rheumatology and Immunology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan ChinaDepartment of Rheumatology and Immunology, Union Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan ChinaAbstract Objectives Tumor necrosis factor‐α (TNF‐α) plays a pivotal role in bone damage associated with inflammatory arthritis such as rheumatoid arthritis (RA). Both systemic lupus erythematosus (SLE) and rheumatoid arthritis exhibit clinical manifestations of inflammatory arthritis, yet the joint bone damage in RA is more severe than that in SLE. The reasons for this differential manifestation remain unclear. This study aimed to determine the role of IgG antibodies in TNF‐α‐induced osteoclastogenesis. Methods We conducted cellular experiments to ascertain whether IgG affects TNF‐α‐induced osteoclastogenesis and validate the role of IgG in TNF‐α‐induced cartilage destruction in mouse models of arthritis through animal studies. Results We found that IgG promoted TNF‐α‐induced osteoclastogenesis by upregulating the expression of tumor necrosis factor receptor 1 (TNFR1) and enhancing the downstream nuclear factor‐kappaB (NF‐κB) signalling pathway. In the TNF‐α‐induced arthritis mouse model, IgG further exacerbated the destruction of articular cartilage. Conclusion Our findings clarified that IgG aggravated TNF‐α‐mediated osteoclastogenesis, further elucidating the mechanistic basis for the divergent manifestations of joint bone damage in SLE and RA.https://doi.org/10.1002/cti2.70034Normal IgGosteoclastogenesisTNFR1TNF‐α |
| spellingShingle | Haifeng Yin Yao Teng Guo‐Min Deng IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathway Clinical & Translational Immunology Normal IgG osteoclastogenesis TNFR1 TNF‐α |
| title | IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathway |
| title_full | IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathway |
| title_fullStr | IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathway |
| title_full_unstemmed | IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathway |
| title_short | IgG promotes TNF‐α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF‐κB signalling pathway |
| title_sort | igg promotes tnf α induced osteoclastogenesis by upregulating the expression of tnfr1 and the nf κb signalling pathway |
| topic | Normal IgG osteoclastogenesis TNFR1 TNF‐α |
| url | https://doi.org/10.1002/cti2.70034 |
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