Key Points: We generated a transgenic mouse model expressing the human IgA1 heavy chain, which has a hinge region with rich -linked glycosylation. After inflammatory stimulation, the mouse model showed elevated galactose-deficient IgA1 levels in the serum. Coupled with complement H factor mutant, the mice model exhibited glomerular lesions, associated with hematuria and albuminuria like IgA nephropathy.
View Article and Find Full Text PDFBackground: IgA nephropathy is a common primary glomerulonephritis caused by mesangial deposition of poly-IgA complexes. The disease follows a variable course of clinical progression, with a high risk of kidney failure. Although no specific therapy is available, enzymatic strategies to clear IgA deposits are being considered for the treatment of rapidly progressive IgA nephropathy.
View Article and Find Full Text PDFMucosal immune regulation is considered a key aspect of immunopathogenesis of IgA nephropathy (IgAN). Direct experimental evidence clarifying the role of intestinal mucosa attributes in IgAN is lacking. In this study, a mouse model was established via multiple low-dose intraperitoneal injections of Lactobacillus casei cell wall extract (LCWE) emulsified with Complete Freund's Adjuvant (CFA).
View Article and Find Full Text PDFBackground And Objectives: Poly-IgA immune complex formation and glomerular deposition play a key role in IgA nephropathy. Our study sought to develop a new methodology for one-step serologic detection of poly-IgA levels.
Design, Setting, Participants, & Measurements: A novel ELISA method using recombinant CD89 as a "capturing" probe was established for detecting poly-IgA immune complex in plasma.
Introduction: Crescents, especially those found at a percentage greater than 50%, are often associated with rapid progression of kidney disease in IgA nephropathy (IgAN). The mechanism of crescents forming in IgAN is still unclear. In this study, we aimed to evaluate whether excess complement activation participates in the formation of crescents in IgAN.
View Article and Find Full Text PDFInt Immunopharmacol
February 2021
Background: There are few studies describing the prevalence and immune features of people with subclinical mesangial immunoglobulin A (IgA) deposition in the Chinese population. We sought to investigate the prevalence of mesangial IgA deposition among kidney donors and the immune characteristics of donors with mesangial IgA deposition.
Methods: Fifty blood-related living donors with zero-hour allograft biopsies obtained at Peking University First Hospital were enrolled.
Introduction: Galactose-deficient IgA1 (Gd-IgA1) and related IgA/IgG immune complexes have been identified as the key drivers in the pathogenesis of IgA nephropathy (IgAN). However, their roles in the development of secondary IgAN are still unknown.
Methods: In this study, we measured the plasma Gd-IgA1 level, IgA/IgG complex, and Gd-IgA1 glomerular deposits in 100 patients with various kinds of secondary IgAN.
Background: Both ABO blood group antigens and pathogenic immunoglobulin A1 (IgA1) in patients with IgA nephropathy (IgAN) are influenced by modifications of N-acetylgalactosamine and galactose. The purpose of this study was to assess whether ABO blood type is associated with galactose-deficient IgA1 (Gd-IgA1) in the progression of kidney disease in patients with IgAN.
Methods: We enrolled 1313 IgAN patients with a median of 44 months follow-up and measured the plasma Gd-IgA1 levels.
Background And Aims: It is recommended that patients with coronary heart disease (CHD) pursue a normal body weight, while the effects of body weight and weight change on prognosis are still controversial. The present study was to assess these effects using a large-scale population with CHD in China.
Methods: A total of 5276 patients with CHD were included from Jan 2000 to Dec 2014.
Lymphocyte function-associated antigen-1 (LFA-1) and macrophage-1 antigen (Mac-1) and their counterreceptors such as intercellular cell adhesion molecules (ICAM-1 and ICAM-2), junctional adhesion molecules (JAM-A, JAM-C), and receptors for advanced glycation end products (RAGE) are crucial for promoting polymorphonuclear leukocyte (neutrophil, PMN) recruitment. The underlying mechanisms of ligand-specific bindings in this cascade remain incompletely known. We compared the dynamic force spectra for various LFA-1/Mac-1-ligand bonds using single-molecule atomic force microscopy (AFM) and tested their functions in mediating PMN recruitment under in vitro shear flow.
View Article and Find Full Text PDFBackground: Both glycated albumin (GA) and glycated hemoglobin (HbA1c) reflect the mean glucose levels. This study was conducted to investigate the relationships among GA, HbA1c, and arterial stiffness in the general population.
Methods: A total of 11,014 participants were included.
Objectives: To assess the effect of baseline body mass index (BMI) status and weight change on mortality in older men with impaired glucose regulation (IGR).
Methods: Eight hundred eighty-five men with IGR aged 60 to 90 were included. Baseline and endpoint weight were measured.
Objective: To investigate associations of novel cardiovascular markers with obesity in a general population.
Methods: A total of 9361 individuals without diabetes or cardiovascular disease were studied between 2009 and 2012 in China. High-sensitivity cardiac troponin T (hs-cTnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP), brachial-ankle pulse wave velocity (baPWV), pulse pressure, and central systolic blood pressure (cSBP) were assessed according to body mass index (BMI) levels and different BMI/metabolic syndrome (MetS) combinations.
Background: The EZSCAN test was recently developed to screen for early dysglycemia through an assessment of sudomotor function. Given the associations of dysglycemia and autonomic dysfunction with the development of arterial stiffness, EZSCAN may also detect early arterial stiffness. The aim of this study was to investigate the association of EZSCAN with arterial stiffness across blood glucose levels.
View Article and Find Full Text PDFInteractions between polymorphonuclear neutrophils (PMNs) and tumor cells have been reported to facilitate the adhesion and subsequent extravasation of tumor cells through the endothelium under blood flow, both of which are mediated by binding β(2)-integrin to intercellular adhesion molecule 1 (ICAM-1). Here the adhesions between human WM9 metastatic melanoma cells, PMNs, and human pulmonary microvascular endothelial cells (HPMECs) were quantified by a gas-driven micropipette aspiration technique (GDMAT). Our data indicated that the cellular binding affinity of PMN-WM9 pair was 3.
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