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Results 41 to 50 of about 37,422 (167)

Immune Complexes Shape the Pathogenicity of Autoantibodies in Systemic Autoimmune Diseases: Insights From an FcγRIIIA‐Reporter Assay

Arthritis &Rheumatology, EarlyView.
Objective Immune complexes (ICs), formed by autoantigen and autoantibody, play a pathogenic role in systemic autoimmune diseases through stimulation of Fcγ receptors (FcγR). However, studies investigating bioactivity of circulating ICs across various diseases remain limited.
Koji Suzuki +8 more
wiley +1 more source

Higher Complement C4 Gene Copy Number Constitutes a Shared Genetic Risk Factor for Giant Cell Arteritis and IgA Vasculitis

Arthritis &Rheumatology, EarlyView.
Objective Low copy number (CN) of complement C4 isoforms and high CN of retroviral HERV‐K elements are known risk factors for many immune‐mediated inflammatory diseases (IMIDs), often showing sex‐biased effects. Here, we assessed whether CN variation within the C4 gene contributes to giant cell arteritis (GCA) and IgA vasculitis (IgAV), two complex ...
Laura Martínez‐Gutiérrez +295 more
wiley +1 more source

C1q-nefropatija: prikazi bolesnika i pregled literature [C1q nephropathy: case reports and literature review] [PDF]

, 2015
C1q nephropathy is considered a form of glomerulonephritis, defined by histological findings of dominant Clq immune deposits in renal biopsy. It is a rare disease, most often manifested in children and young adults. The most common clinical manifestation
Horvatić, Ivica +6 more
core +1 more source

Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity. [PDF]

Immunol Rev
ABSTRACT Post‐translational modifications (PTMs) of proteins are essential to maintain homeostasis as many cellular processes rely on reversible PTMs. However, several PTMs, particularly irreversible PTMs in the extracellular space, can contribute to tissue dysfunction, inflammation, and may even trigger the development of autoimmunity against PTM ...
van Greevenbroek MMJ, Trouw LA.
europepmc +2 more sources

Complement Activation Linked to Type II Interferon Signaling in Still Disease

Arthritis &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

Immunological consequences of C1q and anti-c1q immune complexes in secondary cellular inflammation [PDF]

, 2023
The complement system comprises numerous plasma proteins that are finely orchestrated in a network of at least three separate pathways, namely the classical, lectin, and alternative pathway.
Rabatscher, Pascal
core

Biomaterials for modulating cellular responses of endogenous tendon stem/progenitor cells: A promising avenue for tendon regeneration

BMEMat, EarlyView.
This review comprehensively summarizes emerging biomaterial‐based strategies and underlying mechanisms for modulating endogenous tendon stem/progenitor cells (TSPCs). It offers the most recent insights into TSPC physiology and potential applications of tissue engineering and regenerative medicine in tendons.
Zeyu Zhu +9 more
wiley +1 more source

Von Willebrand Factor Interacts with Surface-Bound C1q and Induces Platelet Rolling. [PDF]

, 2016
Premature atherosclerosis and thrombotic complications are major causes of morbidity and mortality in patients with systemic lupus erythematosus (SLE).
Niemiec, I. +17 more
core +1 more source

Monocyte inflammation and adaptive immune dysfunction in severe Klebsiella pneumoniae pneumonia

iMeta, EarlyView.
Severe Klebsiella pneumoniae pneumonia combines intense inflammation with failure to control infection, yet the cellular basis is unclear. Using a severity‐focused single‐cell atlas of 708,894 peripheral blood mononuclear cells from 100 individuals, complemented by plasma protein measurements and flow cytometry, we show that disease severity redirects ...
Hongquan Chen +23 more
wiley +1 more source

Microbial metabolite indole‐3‐propionic acid preserves astrocytic mitochondrial mitofusin 2 to limit neuroinflammation after traumatic brain injury

Interdisciplinary Medicine, EarlyView.
Following traumatic brain injury, indole‐3‐propionic acid (IPA) directly targets the aryl hydrocarbon receptor on astrocytes in the peri‐lesional cortex; this suppresses interferon regulatory factor 1‐driven transcription of the E3 ubiquitin ligase RFFL (ring finger and FYVE‐like domain containing E3 ubiquitin protein ligase).
Ziwen Zhang +22 more
wiley +1 more source