Results 61 to 70 of about 41,476 (260)
Autoantibodies against Complement C1q Specifically Target C1q Bound on Early Apoptotic Cells [PDF]
The Journal of Immunology, 2009 AbstractAutoantibodies against complement C1q (anti-C1q) are frequently found in patients with systemic lupus erythematosus (SLE). They strongly correlate with the occurrence of severe lupus nephritis, suggesting a pathogenic role in SLE. Because anti-C1q are known to recognize a neoepitope on bound C1q, but not on fluid-phase C1q, the aim of this ...
Bigler, Cornelia +4 more
openaire +3 more sources
Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium [PDF]
, 2008 This study was prompted by the observation that decidual endothelial cells (DECs), unlike endothelial cells (ECs) of blood vessels in normal skin, kidney glomeruli and brain, express surface-bound C1q in physiologic pregnancy. This finding was unexpected,
Agostinis, C. +9 more
core +1 more source
Annals of Clinical and Translational Neurology, EarlyView.ABSTRACT Objective Autosomal dominant progranulin (GRN) pathogenic variants are a genetic cause of frontotemporal lobar degeneration. Though clinical trials for GRN‐related therapies are underway, there is an unmet need for biomarkers that can predict symptom onset and track disease progression.
Taru M. Flagan +46 more
wiley +1 more source
C1q nephropathy developing in a case of gastric carcinoma
Saudi Journal of Kidney Diseases and Transplantation, 2019 C1q is a key intermediary in the classical complement pathway. It is known to be activated by several factors including immunoglobulins and charged molecules and is an initiator of the complement cascade.
Kiran Preet Malhotra +4 more
doaj +1 more source
Structural features of human immunoglobulin G that determine isotype-specific differences in complement activation. [PDF]
, 1993 Although very similar in sequence, the four subclasses of human immunoglobulin G (IgG) differ markedly in their ability to activate complement. Glu318-Lys320-Lys322 has been identified as a key binding motif for the first component of complement, C1q ...
Morrison, SL, Smith, RI, Tao, MH
core
Cerebral complement C1q activation in chronic Toxoplasma infection [PDF]
Brain, Behavior, and Immunity, 2016 Exposure to the neurotropic parasite, Toxoplasma gondii, causes significant brain and behavioral anomalies in humans and other mammals. Understanding the cellular mechanisms of T. gondii-generated brain pathologies would aid the advancement of novel strategies to reduce disease.
Robert H. Yolken +10 more
openaire +3 more sources
Annals of Clinical and Translational Neurology, EarlyView.ABSTRACT Introduction Neuronal pentraxin 2 (NPTX2) is a synaptic protein involved in synaptic plasticity and regulation of neuronal excitability. Lower baseline cerebrospinal fluid (CSF) NPTX2 levels have been shown to be associated with an earlier onset of mild cognitive impairment (MCI), a pre‐dementia syndrome, even after CSF Alzheimer's Disease (AD)
Juan P. Vazquez +12 more
wiley +1 more source
International Journal of Retina and Vitreous, 2022 Geographic atrophy (GA) secondary to age-related macular degeneration (AMD) is a retinal neurodegenerative disorder. Human genetic data support the complement system as a key component of pathogenesis in AMD, which has been further supported by pre ...
Ted Yednock +2 more
doaj +1 more source
Glomerular C1q deposition and serum anti-C1q antibodies in anti-glomerular basement membrane disease [PDF]
, 2013 BACKGROUND: Anti-glomerular basement membrane (GBM) disease is a well-known antibody-induced autoimmune disease. A few patients have glomerular C1q deposition, but it is usually absent on renal histopathology.
Feng Yu +5 more
core +1 more source
Biomaterial Strategies for Targeted Intracellular Delivery to Phagocytes
Advanced Functional Materials, EarlyView.Phagocytes are essential to a functional immune system, and their behavior defines disease outcomes. Engineered particles offer a strategic opportunity to target phagocytes, harnessing inflammatory modulation in disease. By tuning features like size, shape, and surface, these systems can modulate immune responses and improve targeted treatment for a ...
Kaitlyn E. Woodworth +2 more
wiley +1 more source