Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
The discovery of gut-specific leukocytes and the ability to modulate their function has been a groundbreaking development in the treatment of inflammatory bowel disease. Drugs target the interaction between lymphocytes and endothelial cells via integrins and their ligand cellular adhesion molecules. Safety, efficacy and sustainability of effect are key to this drug class, notwithstanding the association of natalizumab with fatal polyoma virus infection. Vedolizumab (2014) now licensed for the treatment of Crohn's disease around the world provides gut-specific immunosuppression. Targets for modulators of leukocyte trafficking include (examples in brackets) ICAM-1 (alicaforsen, efalizumab); MAdCAM-1 (PF-00547 659); α4 and related receptors (abrilumab, etrolizumab, natalizumab, vedolizumab); chemokine receptor CCR9 (vercirnon); and sphingosine 1-phosphate receptors (etrasimod, fingolimod, ozanimod). Oral and subcutaneous therapies are in development. The safety, efficacy and practice points of licensed drugs are discussed, in addition to initial results from therapeutic trials.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bpg.2019.05.004 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Circadian Clock: A Regulator of Immunity in Autoimmune Diseases.
Immun Inflamm Dis
September 2025
School of Clinical Medicine, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Aim: Autoimmune diseases, characterized by the immune system mistakenly attacking the body's own tissues, are a growing global concern, with increasing prevalence. The circadian clock is a fundamental regulator of physiological processes, critically modulating immune functions. This review explores the intricate connections between circadian rhythms and immune responses in autoimmune pathogenesis and how disruptions exacerbate disease.
View Article and Find Full Text PDFChronic social defeat stress induces meningeal neutrophilia via type I interferon signaling in male mice.
Nat Commun
September 2025
National Institute of Mental Health, Bethesda, MD, USA.
Inflammation is increasingly recognized as a risk factor for psychiatric disorders. Animal models of stress and stress-related disorders are associated with blood neutrophilia. The mechanistic relevance of this to symptoms or behavior is unclear.
View Article and Find Full Text PDFPharmacological inhibition of the CCL2-CCR2 axis fails to reduce inflammation in a rat model of acute lung injury.
Sci Rep
August 2025
Critical Care Research Center, Parc Taulí Hospital Universitari, Institut d'Investigació I Innovació Parc Taulí (I3PT-CERCA), Universitat Autònoma de Barcelona, Sabadell, Spain.
New therapeutic approaches are needed to regulate inflammation and control monocyte recruitment in acute respiratory distress syndrome (ARDS). Excessive monocyte influx into the alveolar space can exacerbate lung damage, worsening patient outcomes. Delaying or reducing monocyte recruitment into the alveoli space after the injury has been proposed as a strategy to balance the inflammatory response and mitigate lung damage.
View Article and Find Full Text PDFMYADM Activates RhoA-Mediated Amoeboid Migration to Drive Metastasis.
Cancer Res
August 2025
National Health Research Institutes, Miaoli County, Taiwan.
Metastasis, the leading cause of cancer-related mortality, remains the most critical challenge in cancer treatment. Cancer cells can adopt amoeboid migration to facilitate metastasis, highlighting the need elucidate the molecular pathways regulating the amoeboid migration phenotype. Here, we identified that MYADM, a transmembrane protein expressed during myeloid cell maturation, enabled cancer cells to acquire amoeboid migration plasticity, promoting metastasis and contributing to poor patient outcomes.
View Article and Find Full Text PDFAltered Immune Profiles in Non-Failing Heart Donors With Induced Long QT Syndrome: A Potential Risk Factor for Cardiac Allograft Vasculopathy.
Clin Transplant
August 2025
Department of Cardiothoracic Vascular Surgery, People's Hospital of Deyang City, Deyang, Sichuan, P.R. China.
Introduction: Cardiac allograft vasculopathy (CAV) develops more aggressively in recipients of hearts from brain-dead (BD) donors with induced long QT syndrome (iLQTS), yet the underlying mechanisms remain poorly understood. In this study, we employ a multi-omics and experimental framework to explore the role of neuro-immune interactions in non-failing donor hearts affected by iLQTS.
Methods: Single-nuclei RNA sequencing (snRNA-seq) compared four iLQTS and four non-arrhythmic non-failing donor hearts.