Arthritis & rheumatology (Hoboken, N.J.) · 2026
Integrative Multiomics Approaches Identify Biomarkers Associated With Progression From Arthralgia to Rheumatoid Arthritis.
СтатьяНазвание и аннотация: Перевод в очереди
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Li Min, Han Yipeng, Zhan Minghua, Zhang Xiaomei, Wang Haoxiang, Wang Xi, Zhao Xuyang, Cheng Gong, Yu Siyue, Huang Bo, Yan Rui, Liu Qinghong, Xing Xiaoyan, Zang Sitian, Chi Jing, Jin Yuebo, Jia Yuan, Su Yin, Wang Qingwen, Yu Xiaobo, Li Zhanguo, Liu Yudong, He Jing
Аннотация
OBJECTIVE: Arthralgia, an early manifestation preceding definite rheumatoid arthritis (RA), represents a critical window to identify high-risk individuals and implement timely interventions. However, the immunopathologic mechanisms underlying the transition from arthralgia to established RA remain incompletely defined.
METHODS: We employed a multiomics strategy integrating peripheral immune cell phenotyping, serum proteomics, and autoantibody profiling to investigate the immunopathologic continuum from preclinical to established RA. A prospective cohort of 346 patients with recent-onset arthralgia was enrolled. Participants included healthy controls, self-limiting arthralgia (SLA), arthralgia at risk of RA (at-risk individuals, ARI), early RA, and established RA. RA development in ARI was ascertained through 24-month follow-up.
RESULTS: Compared with SLA, ARI showed immune dysregulation, including reduced Treg cells and a lower Treg/Th17 cell ratio, with related changes persisting into early RA. Serum proteomics revealed upregulation of C5, α-1-B glycoprotein, RPUSD4, WDR87, and FUBP2, which showed inverse associations with Treg cells. Autoantibody profiling identified stage-specific reactivity, with ARI showing elevated antibodies against stress-related proteins. Within 24 months, 18.4% of ARI progressed to RA (converters). Baseline immunophenotypic differences between converters and nonconverters were comparable, whereas longitudinal paired analyses revealed a reduction in Treg cells and Treg/Th17 cell ratio. Treg/Th17 cell ratio (area under the curve [AUC] 0.734) outperformed anti-cyclic citrullinated peptide (CCP; AUC 0.611) in discriminating ARI from SLA, particularly in patients who are anticitrullinated peptide antibodies negative (AUC 0.729). Combining Treg cells, anti-CCP and Treg/Th17 cell ratio improved classification performance (AUC 0.783).
CONCLUSION: These findings delineate a critical transition from reversible immune dysregulation to established autoimmunity along the arthralgia-RA continuum, suggesting that Treg cell-related dysregulation may be associated with progression toward persistent inflammatory arthritis.
METHODS: We employed a multiomics strategy integrating peripheral immune cell phenotyping, serum proteomics, and autoantibody profiling to investigate the immunopathologic continuum from preclinical to established RA. A prospective cohort of 346 patients with recent-onset arthralgia was enrolled. Participants included healthy controls, self-limiting arthralgia (SLA), arthralgia at risk of RA (at-risk individuals, ARI), early RA, and established RA. RA development in ARI was ascertained through 24-month follow-up.
RESULTS: Compared with SLA, ARI showed immune dysregulation, including reduced Treg cells and a lower Treg/Th17 cell ratio, with related changes persisting into early RA. Serum proteomics revealed upregulation of C5, α-1-B glycoprotein, RPUSD4, WDR87, and FUBP2, which showed inverse associations with Treg cells. Autoantibody profiling identified stage-specific reactivity, with ARI showing elevated antibodies against stress-related proteins. Within 24 months, 18.4% of ARI progressed to RA (converters). Baseline immunophenotypic differences between converters and nonconverters were comparable, whereas longitudinal paired analyses revealed a reduction in Treg cells and Treg/Th17 cell ratio. Treg/Th17 cell ratio (area under the curve [AUC] 0.734) outperformed anti-cyclic citrullinated peptide (CCP; AUC 0.611) in discriminating ARI from SLA, particularly in patients who are anticitrullinated peptide antibodies negative (AUC 0.729). Combining Treg cells, anti-CCP and Treg/Th17 cell ratio improved classification performance (AUC 0.783).
CONCLUSION: These findings delineate a critical transition from reversible immune dysregulation to established autoimmunity along the arthralgia-RA continuum, suggesting that Treg cell-related dysregulation may be associated with progression toward persistent inflammatory arthritis.