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...

Full description

Saved in:
Bibliographic Details
Main Authors: Haifeng Yin, Yao Teng, Guo‐Min Deng
Format: Article
Language:English
Published: Wiley 2025-01-01
Series:Clinical & Translational Immunology
Subjects:
Online Access:https://doi.org/10.1002/cti2.70034
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849716982412214272
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
work_keys_str_mv AT haifengyin iggpromotestnfainducedosteoclastogenesisbyupregulatingtheexpressionoftnfr1andthenfkbsignallingpathway
AT yaoteng iggpromotestnfainducedosteoclastogenesisbyupregulatingtheexpressionoftnfr1andthenfkbsignallingpathway
AT guomindeng iggpromotestnfainducedosteoclastogenesisbyupregulatingtheexpressionoftnfr1andthenfkbsignallingpathway