Results 71 to 80 of about 2,283,992 (229)

Complement Activation Linked to Type II Interferon Signaling in Still Disease

open access: yesArthritis &Rheumatology, EarlyView.
Objective Still disease (SD) is an autoinflammatory syndrome characterized by innate immune dysregulation. Although complement can drive inflammation, its involvement in SD remains to be defined. Thus, we aimed to assess complement activation in SD. Methods Complement was assessed using transcriptomic, proteomic, and in vitro approaches. RNA sequencing
Freya M. C. H. Huijsmans   +115 more
wiley   +1 more source

Clustering reveals diagnostic overlap between Still’s disease and a hyperinflammatory subset of seronegative rheumatoid arthritis

open access: yesScientific Reports
Still’s disease (SD) and rheumatoid arthritis (RA), particularly seronegative RA, may overlap clinically and biologically, complicating diagnosis. We explored data-driven overlaps between SD, seronegative RA, and seropositive RA using unsupervised ...
Alexandre Mercier-Guery   +8 more
doaj   +1 more source

Real-Life Data on the Efficacy of Canakinumab in Patients with Adult-Onset Still’s Disease

open access: yesMediators of Inflammation, 2020
Background. Interleukin-1 inhibition has revealed to be a successful treatment approach for patients with adult-onset Still’s disease (AOSD). However, real-life experience is focused on the use of anakinra, while data about canakinumab (CAN) are mainly ...
Antonio Vitale   +12 more
doaj   +1 more source

Persistent Interleukin‐18 Fuels Expansion of CD38+HLA‐DR+CD8+ T Cells in Still Disease and Macrophage Activation Syndrome

open access: yesArthritis &Rheumatology, EarlyView.
Objective Still disease (SD) is an autoinflammatory disorder characterized by remarkably high interleukin‐18 (IL‐18) levels. Increasing evidence suggests that adaptive immunity also contributes to its pathogenesis, particularly in refractory courses. Macrophage activation syndrome (MAS), one of SD's most severe complications, is associated with further
Greta Rogani   +17 more
wiley   +1 more source

Interleukin-1, inflammasome and autoinflammatory diseases

open access: yes, 2018
International audienceInterleukin-1 is a major cytokine of innate immunity and inflammation. It exerts various systemic effects during the inflammatory response, such as fever induction, thrombopoiesis and granulopoiesis, or leukocyte recruitment.
Barba, T.   +8 more
core   +1 more source

Inflammation Unchecked: Concurrent Kawasaki Disease and Stevens‐Johnson Syndrome in an 18‐Month‐Old Child

open access: yes
Arthritis Care &Research, EarlyView.
Catherine Deffendall   +6 more
wiley   +1 more source

Human Monocytic Models Reveal Genotype‐Dependent Inflammatory Programs in VEXAS Syndrome

open access: yesArthritis &Rheumatology, EarlyView.
Objective VEXAS syndrome is a severe X‐linked autoinflammatory disorder caused by somatic mutations in ubiquitin‐like modifier activating enzyme 1 (UBA1), with clinical outcomes that vary by UBA1 genotype. We aimed to elucidate genotype‐specific inflammatory programs and identify potential therapeutic targets.
Kana Higashitani   +10 more
wiley   +1 more source

Shared and Distinguishing Features of Late‐Onset Rheumatic Diseases Fulfilling Polymyalgia Rheumatica Classification Criteria

open access: yesArthritis &Rheumatology, Accepted Article.
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Kerem Abacar   +5 more
wiley   +1 more source

Predictive factors for therapeutic response and cluster analysis in syndrome of undifferentiated recurrent fever (SURF)

open access: yesRMD Open
Introduction: Syndrome of undifferentiated recurrent fever (SURF) refers to a group of recurrent fevers without a clear monogenic cause. Clinical spectrum, treatment response predictors and management strategies remain unclear. Objective: This study aims
Marco Gattorno   +15 more
doaj   +1 more source

Autoinflammatory diseases: An immunologist’s view

open access: yesСовременная ревматология, 2015
Autoinflammatory syndromes (AISs) are a heterogeneous group of genetically determined diseases, whose basis is the dysregulated mechanisms of inflammation.
A. Yu. Shcherbina
doaj   +1 more source

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