From patients with arthralgia, pre-RA and recently diagnosed RA: what is the current status of understanding RA pathogenesis?

Molendijk, Marlieke; Hazes, Johanna M. W.; Lubberts, Erik

doi:10.1136/rmdopen-2016-000256

Cited by 34 publications

(19 citation statements)

References 45 publications

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“…It is important to bear in mind that RA is a dynamic disease in its development, so a complete understanding of how RA develops over time is important to set up therapies that prevent disease progression rather than treating its symptoms [ 35 ]. The importance of the neuroimmune network in joint homeostasis has been shown.…”

Section: An Introduction To the Physiopathology Of Rheumatoid Arthmentioning

confidence: 99%

The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis

Villanueva‐Romero

Gutiérrez‐Cañas

Carrión

et al. 2018

Journal of Immunology Research

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Genetic background, epigenetic modifications, and environmental factors trigger autoimmune response in rheumatoid arthritis (RA). Several pathogenic infections have been related to the onset of RA and may cause an inadequate immunological tolerance towards critical self-antigens leading to chronic joint inflammation and an imbalance between different T helper (Th) subsets. Vasoactive intestinal peptide (VIP) is a mediator that modulates all the stages comprised between the arrival of pathogens and Th cell differentiation in RA through its known anti-inflammatory and immunomodulatory actions. This “neuroimmunopeptide” modulates the pathogenic activity of diverse cell subpopulations involved in RA as lymphocytes, fibroblast-like synoviocytes (FLS), or macrophages. In addition, VIP decreases the expression of pattern recognition receptor (PRR) such as toll-like receptors (TLRs) in FLS from RA patients. These receptors act as sensors of pathogen-associated molecular pattern (PAMP) and damage-associated molecular pattern (DAMP) connecting the innate and adaptive immune system. Moreover, VIP modulates the imbalance between Th subsets in RA, decreasing pathogenic Th1 and Th17 subsets and favoring Th2 or Treg profile during the differentiation/polarization of naïve or memory Th cells. Finally, VIP regulates the plasticity between theses subsets. In this review, we provide an overview of VIP effects on the aforementioned features of RA pathology.

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Section: An Introduction To the Physiopathology Of Rheumatoid Arthmentioning

confidence: 99%

The Anti-Inflammatory Mediator, Vasoactive Intestinal Peptide, Modulates the Differentiation and Function of Th Subsets in Rheumatoid Arthritis

Villanueva‐Romero

Gutiérrez‐Cañas

Carrión

et al. 2018

Journal of Immunology Research

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“…There is evidence of T-cell-mediated immune dysregulation in RA irrespective of autoantibody production [24]. Serotype distinctions include differences in immune cells subtypes, cytokines and chemokines [25].…”

Section: Rheumatoid Arthritis: Pathogenesismentioning

confidence: 99%

“…The synovium in patients with established RA displays an inflammatory infiltrate composed of a heterogeneous set of immune cells. Neutrophils present in the synovial fluid have an extended lifespan and feature an enhanced production of reactive oxygen species and neutrophil extracellular traps (NETosis) [25]. Synovial T cells, especially CD28-CD4+ T cells are autoreactive, produce interferon-gamma (IFN-γ) and are resistant to apoptosis [26].…”

Section: Rheumatoid Arthritis: Pathogenesismentioning

confidence: 99%

Diagnostic Challenges and Management Update in Rheumatoid Arthritis

Boldeanu¹,

Ionescu²,

Popoviciu³

et al. 2020

Rheumatoid Arthritis - Other Perspectives Towards a Better Practice

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Rheumatoid arthritis is a chronic, systemic inflammatory disease, with certain evidence of multiple factors involved, but also with the strong autoimmune component, leading to a high potential for disability, through synovial inflammation and joint destruction. Diagnostic methods and management possibilities have recently improved, thus leading to a better outcome, based on the treat to target recommendation. Although biologic agents represent efficient therapeutic agents, in the last few years, the advances in understanding the mediators involved in rheumatoid arthritis pathogenesis have provided new targeted therapies, represented by small molecule inhibitors against the Janus kinases that contribute in the signaling pathways of various cytokine receptors.

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“…Получены данные, создающие теоретические предпосылки для применения РТМ с целью первичной профилактики РА у пациентов с высоким риском развития этого заболевания -при так называмой «клинически подозрительной артралгии» [41,42]. По данным многоцентрового РПКИ PRAIRI (Prevention of clinically manifest Rheumatoid ArthrItis by B Cell DiRected Therapy In the Earliest Phase of the Disease), в которое были включены пациенты с артралгиями и положительными результатами определения АЦБ и РФ, однократная инфузия РТМ достоверно замедляет развитие РА [43].…”

Section: ревматоидный артритunclassified