Background: TNF-like cytokine 1A (TL1A)-mediated interactions are involved in atheromatic plaque formation. In stable coronary artery disease (CAD) we examined whether circulating TL1A levels correlate with coronary and/or peripheral atherosclerosis extent and predict future cardiovascular events.

Methods: In this cross-sectional study, peripheral vascular studies and TL1A serum measurements were performed in 122 consecutive patients with angiographically confirmed CAD who were followed for a median of 41.9 months. TL1A levels were compared against controls (n = 63) and 20 patients with acute coronary syndrome (ACS).

Results: TL1A was higher in ACS than the 2 other groups (p < 0.001). In stable CAD, after adjustment for traditional risk factors independent positive correlations between TL1A serum levels and reflected waves (p = 0.049), and carotid atheromatic plaque score (p = 0.049) were evident. In stable patients with a history of ACS, TL1A levels correlated with worse endothelial function (p = 0.006), extent of CAD assessed by Gensini score (p = 0.042), and cardiac mortality (p = 0.051).

Conclusions: This pilot study suggests that serum TL1A measurements are of clinical value in CAD. Studies on the pathogenetic role of TL1A in atherosclerosis and its sequelae are warranted.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.cyto.2014.12.016DOI Listing

Publication Analysis

Top Keywords

tl1a levels
12
tnf-like cytokine
8
reflected waves
8
atherosclerosis extent
8
extent predict
8
stable coronary
8
coronary artery
8
artery disease
8
atheromatic plaque
8
tl1a
8

Similar Publications

Objective: To investigate serum TL1A levels and their correlation with Th17 cells, IL-17, and IL-21 in children with Graves' disease (GD).

Methods: Thirty-seven children (12 males and 25 females) aged 9-14 years with newly diagnosed and untreated GD were enrolled in this study. Serum TL1A, IL-17, and IL-21 levels were measured using enzyme-linked immunosorbent assay (ELISA).

View Article and Find Full Text PDF

RIPK3 and caspase-8 interpret cytokine signals to regulate ILC3 survival in the gut.

Mucosal Immunol

December 2024

Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology & Hepatology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Department of Microbiology & Immunology, Weill Cornell Medicine, Cornell University, New York, NY, USA; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA. Electronic address:

Group 3 innate lymphoid cells (ILC3s) are abundant in the developing or healthy intestine to critically support tissue homeostasis in response to microbial colonization. However, intestinal ILC3s are reduced during chronic infections, colorectal cancer, or inflammatory bowel disease (IBD), and the mechanisms driving these alterations remain poorly understood. Here we employed RNA sequencing of ILC3s from IBD patients and observed a significant upregulation of RIPK3, the central regulator of necroptosis, during intestinal inflammation.

View Article and Find Full Text PDF

Background: The treatment options for inflammatory bowel disease (IBD) have grown over the last years. However, a significant fraction of patients either do not respond to their treatment or lose response over time.

Summary: Future treatment options could include antibodies that target the tumor necrosis factor-like ligand 1A (TL1A).

View Article and Find Full Text PDF
Article Synopsis
  • Airway epithelial cell necroptosis plays a significant role in worsening asthma and allergic inflammation, with the TL1A/DR3 pathway linked to potential therapeutic effects.
  • Research showed increased levels of necroptosis markers in asthmatic patients and OVA-induced mice, suggesting that targeting necroptosis can reduce airway inflammation and improve barrier function.
  • Blocking necroptosis through genetic knockout or pharmacological inhibition led to decreased inflammation and recovery of airway integrity, implicating TL1A as a key player in airway epithelial dysfunction in asthma.
View Article and Find Full Text PDF

Protective effects of DcR3-SUMO on lipopolysaccharide-induced inflammatory cells and septic mice.

Int J Biol Macromol

August 2024

Department of Neurosurgery & Neurocritical Care, Huashan Hospital, Fudan University, Shanghai 200040, China. Electronic address:

Despite the high mortality rate associated with sepsis, no specific drugs are available. Decoy receptor 3 (DcR3) is now considered a valuable biomarker and therapeutic target for managing inflammatory conditions. DcR3-SUMO, an analog of DcR3, has a simple production process and high yield.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!