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  • Online Resource  (2)
  • Wiley  (2)
  • Medicine  (2)
  • XA 13160  (2)
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  • Online Resource  (2)
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  • Wiley  (2)
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  • Medicine  (2)
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  • XA 13160  (2)
  • 1
    In: APMIS, Wiley, Vol. 131, No. 9 ( 2023-09), p. 498-509
    Abstract: Rheumatoid arthritis (RA) is a common autoimmune disease. Janus kinase inhibitors (JAKi) have been approved for the treatment of RA; however, the impact of JAKi on immune cells remains inconclusive. This study investigated the response of immune cells to JAKi treatment to identify biomarkers by which to evaluate and predict clinical outcomes. Blood samples were collected from RA patients before and after JAKi treatment for the analysis of immunophenotypes. Our results revealed that JAKi mainly inhibited Fas+ T cell subsets. The percentage changes of Th Fas+ and Naive Th Fas+ cells were positively correlated with the 28‐joint Disease Activity Score with erythrocyte sedimentation rate (DAS28‐ESR) values. Following treatment, moderate response (MR) RA patients presented a decrease in the number of Naive Th Fas+ cells (p = 0.0001). Initial percentages of 14 T cell and 20 B cell subsets were correlated with percentage changes in DAS28‐ESR. Overall, 16 cell subsets presented significant differences between the non‐response (NR) and MR groups. Excluding the multicollinearity of the immune cells, we constructed a JAKi treatment response prediction index (JRPI) using 5 subsets of T/B cells, the results of which were strongly correlated with percentage changes in DAS28‐ESR (receiver operating characteristic curve of 1). Note that the NR group was clearly distinguished from the MR group (p = 0.0167). In conclusion, the efficacy of JAKi can be attributed mainly to the suppression of Fas+ T cell subsets. A positive correlation was shown between the therapeutic efficacy of JAKi and the percentage changes in both Th Fas+ cells and Naive Th Fas+ cells. Furthermore, the proposed JRPI could potentially be used as an indicator to predict the efficacy of JAKi prior to treatment in RA patients. These findings may contribute to the development of personalized treatment strategies for RA patients using JAKi.
    Type of Medium: Online Resource
    ISSN: 0903-4641 , 1600-0463
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2098213-6
    detail.hit.zdb_id: 913841-9
    SSG: 12
    Location Call Number Limitation Availability
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  • 2
    In: APMIS, Wiley, Vol. 132, No. 6 ( 2024-06), p. 382-415
    Abstract: Rheumatoid arthritis (RA) is a multifaceted autoimmune disorder characterized by chronic inflammation and joint destruction. Recent research has elucidated the intricate interplay between gut microbiota and RA pathogenesis, underscoring the role of microbiota‐derived metabolites as pivotal contributors to disease development and progression. The human gut microbiota, comprising a vast array of microorganisms and their metabolic byproducts, plays a crucial role in maintaining immune homeostasis. Dysbiosis of this microbial community has been linked to numerous autoimmune disorders, including RA. Microbiota‐derived metabolites, such as short‐chain fatty acids (SCFAs), tryptophan derivatives, Trimethylamine‐N‐oxide (TMAO), bile acids, peptidoglycan, and lipopolysaccharide (LPS), exhibit immunomodulatory properties that can either exacerbate or ameliorate inflammation in RA. Mechanistically, these metabolites influence immune cell differentiation, cytokine production, and gut barrier integrity, collectively shaping the autoimmune milieu. This review highlights recent advances in understanding the intricate crosstalk between microbiota metabolites and RA pathogenesis and also discusses the potential of specific metabolites to trigger or suppress autoimmunity, shedding light on their molecular interactions with immune cells and signaling pathways. Additionally, this review explores the translational aspects of microbiota metabolites as diagnostic and prognostic tools in RA. Furthermore, the challenges and prospects of translating these findings into clinical practice are critically examined.
    Type of Medium: Online Resource
    ISSN: 0903-4641 , 1600-0463
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 2098213-6
    detail.hit.zdb_id: 913841-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
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