Objective: As a member of interleukin-12 family, interleukin-35 (IL-35) plays an important regulatory role in immune response. The relationship between IL-35 and idiopathic membranous nephropathy (IMN) is still unclear, and the purpose of this study is to clarify the relationship between IL-35 and disease activity and remission of IMN.
Methods: This study was a single-center, retrospective study in which all patients were diagnosed with IMN by renal biopsy or aPLA2R titer and treated with Mahuang Fuzi and Shenzhuo Decoction (MFSD). A follow-up was conducted with the endpoint of clinical complete or partial remission (CR+PR). Levels of serum IL-35 were measured and its relationship with IMN remission were analyzed. The regulatory T cell (Treg) and inducible IL-35 producing Tregs (iTR35) in peripheral blood of IMN patients were detected by flow cytometry.
Results: A total of 76 IMN patients (age 51.95 ± 13.29) were followed-up for 18 (12, 24) months. The level of serum IL-35 in all patients increased after treatment, but the degree of increase in remission group was significantly higher than that in no remission (NR) group (117.6% 83.7%, <0.01). The baseline IL-35 level in remission group was higher than that in NR group (174.87 .151.87 pg/ml, =0.016). Cox regression analysis showed that baseline IL-35 level was a independent risk factor for IMN remission (HR 1.081, 95%CI 1.048-1.116, <0.001). Patients with baseline IL-35 lower than the lower quartile (≤145.49 pg/ml) had an average remission time twice as long as those with baseline IL-35 higher than the upper quartile (> 203.05 pg/ml) (12mon . 24mon, <0.01). The baseline IL-35 can predict the remission time of IMN patients with either aPLA2R positive (AUC=0.673) or negative (AUC=0.745). Analysis of 18 patients with IMN showed that IL-35 level had a higher correlation with iTR35, but not Treg (r=0.613, <0.05).
Conclusions: The level of IL-35 in patients with IMN showed an increasing trend with the progress of treatment, and the baseline IL-35 could predict the remission time of IMN patients, including those patients with negative aPLA2R. The level of IL-35 is related to the number of iTR35 cells.
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http://dx.doi.org/10.3389/fimmu.2022.926368 | DOI Listing |
Cureus
December 2024
Nephrology, Archbold Hospital, Alabama College of Osteopathic Medicine, Thomasville, USA.
Membranous nephropathy due to a positive PLA2R marker is an idiopathic cause of membrane nephropathy, characterized as an autoimmune attack on the kidney at the PLA2R receptor. Autoantibodies attack the PLA2R receptor, leading to nephrotic syndrome and eventually leading to end-stage renal failure, as in our case. We present a case that involves a patient who presented to the nephrology clinic with nephrotic range proteinuria and a history of HIV.
View Article and Find Full Text PDFAm J Ophthalmol
January 2025
Department of biomedical sciences, Humanitas University, Pieve Emanuele, Milan, Italy.; Ophthalmology Department, Humanitas Gavazzeni, Bergamo, Italy.
Purpose: To investigate the incidence, clinical spectrum and pathophysiology of microcystoid macular edema (MME) in two cohorts of patients with epiretinal membrane (ERM) and idiopathic full thickness macular hole (FTMH).
Design: Single-center, Retrospective, interventional, cohort study.
Methods: Review of clinical charts, structural and en-face optical coherence tomographty (OCT) and fluorescein angiography (FA) imaging of ERM and FTMH eyes which underwent surgery with pars plana vitrectomy and internal limiting membrane (ILM) peel, with a minimum follow-up of 6 months.
Sci Rep
January 2025
Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
Autism spectrum disorder (ASD) comprises alterations in brain anatomy and physiology that ultimately affect information processing and behavior. In most cases, autism is considered idiopathic, involving alterations in numerous genes whose functions are not extensively documented. We evaluated the C58/J mouse strain as an idiopathic model of ASD, emphasizing synaptic transmission as the basis of information processing.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Front Pharmacol
December 2024
Renal Division, State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Background: Particulate matter (PM2.5) has been implicated in the development of membranous nephropathy (MN), but the underlying mechanism has yet to be fully understood. Oxidative stress is an essential factor of PM2.
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