Patients with atopic dermatitis were found to have an about 7-fold increased spontaneous proliferative response of peripheral blood lymphocytes and an about 4-fold elevation of CD3-dependent lymphocyte transformation as compared to normal controls. The CD3-dependent lymphocyte response in patients with severe atopic dermatitis lesions was increased to a lower degree than in those with mild skin lesions. Despite a highly increased CD3-dependent lymphocyte response, the extracellular matrix proteins could induce further co-stimulation of lymphocytes in patients with atopic dermatitis, similar to that in normal controls. However, co-activation by type IV collagen was markedly increased in patients with severe lesions, whereas co-stimulations by both type I collagen and fibronectin were decreased in patients with mild lesions. This finding reflects presumably the changes in lymphocyte subpopulations and their activities related to the recirculation of these cells through the active skin lesions and to the contact of T cells with extracellular matrix proteins. The percentage of CD26-positive lymphocytes was also significantly (p < 0.05) increased in patients with severe atopic dermatitis. These data indicate that helper T cells are excessively activated in atopic dermatitis and that the function of beta-1-integrin receptors underlying the extracellular matrix protein-mediated co-activation of CD3-dependent lymphocyte responses is modified by disease severity.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2340/0001555575353356 | DOI Listing |
Atopic dermatitis (AD) is a prevalent condition that has been associated with stress, but epidemiologic data on the impact of both common and severe childhood stressors are limited. Our objective was to evaluate the impact of stressful life events throughout early childhood on AD activity and severity. We conducted a longitudinal cohort study of 13,972 children ages 1 to 8.
View Article and Find Full Text PDFClin Immunol
January 2025
Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710032, China. Electronic address:
NLRX1 is an important regulator of inflammatory signaling in innate immune cells. Recent studies indicate NLRX1 activation may be a novel mechanism for inflammatory diseases, however, it has not been explored in atopic dermatitis (AD). Our study aims to investigate the potential role of NLRX1 in the pathogenesis of AD.
View Article and Find Full Text PDFBr J Dermatol
January 2025
Centre of Evidence Based Dermatology, School of Medicine, Faculty of Medicine & Health Sciences, University of Nottingham, UK.
Background: Randomised controlled trials (RCTs) evaluating new systemic treatments for atopic dermatitis (AD) have increased dramatically over the last decade. These trials often incorporate topical therapies either as permitted concomitant or rescue treatments. Differential use of these topicals post-randomisation introduces potential bias as they may nullify or exaggerate treatment responses.
View Article and Find Full Text PDFAm J Rhinol Allergy
January 2025
Department of Otolaryngology-Head and Neck Surgery, University of California, Irvine, Orange, CA, USA.
Background: Dupilumab was first approved by the United States Food and Drug Administration in 2017 for atopic dermatitis and has since been approved for many other indications. The use of dupilumab has grown, but industry payments to physicians have yet to be explored.
Objective: The study objective is to characterize the change in payments by pharmaceutical companies to physicians for dupilumab-related promotional activities.
Br J Dermatol
January 2025
Laboratory of Social Pharmacy and Public Health, Faculty of Pharmacy, University of Coimbra, Portugal, Coimbra, Portugal.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!