
European Cytokine Network is an electronic journal that publishes original research articles, review articles, etc., on a quarterly basis to provide an essential bridge between researchers and clinicians with an interest in the field of cytokines.
It has become a must-read for specialists in the field thanks to its swift publication and international circulation.
Science Citation Index Expanded (SCIE): 2024 Impact Factor 1.2; Scopus: Citescore 3.3 (2024), SNIP (Source Normalized Impact per Paper): 0.342 (2024); PubMed/Medline; Embase; Google Scholar, etc.
Effective 2026, the European Cytokine Network (ECN) will be published by Tech Science Press (TSP). This transition is designed to enhance the journal's academic impact and global visibility while ensuring an improved publishing experience for researchers. The journal's aims, scope, and formatting guidelines will remain unchanged. The journal's Editor-in-Chief, Prof. Hans Yssel, and the editorial board will continue to lead the journal toward an even more successful future.
We sincerely appreciate the continued support of our contributors, reviewers, readers, and Editorial Board Members, and we look forward to advancing cytokine research together in this new chapter.
Open Access
REVIEW
European Cytokine Network, Vol.37, No.1, pp. 1-11, 2026, DOI:10.32604/ecn.2026.0ECN78096 - 13 April 2026
Abstract The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that exhibits antagonistic pleiotropy, mediating both protective and detrimental cellular effects depending on the ligand and context. AhR can be activated by a variety of endogenous and exogenous stimuli, including environmental pollutants, UVB radiation, heme, arachidonic acid metabolites, gut microbiota–derived compounds, and xenobiotics. Upon activation, AhR translocates to the nucleus, where it dimerizes with the aryl hydrocarbon receptor nuclear translocator (ARNT) and binds to xenobiotic response elements, inducing the expression of genes involved in xenobiotic metabolism, oxidative stress responses, and inflammatory signaling. In addition to… More >
Open Access
REVIEW
European Cytokine Network, Vol.37, No.1, pp. 13-24, 2026, DOI:10.32604/ecn.2026.078458 - 13 April 2026
Abstract Cytokine storm syndromes have become a much-invoked concept to describe severe immunopathology in infectious, inflammatory, and iatrogenic diseases, but the concept is poorly defined and often mechanistically imprecise. High levels of systemic cytokines have often been viewed as indicators of immune dysfunction, and based on this notion, therapeutic interventions focused on general cytokine inhibition are proposed. Nevertheless, a growing number of clinical and experimental data dispute the notion that hypercytokinemia is necessarily pathological. The present paper reconsiders cytokine storm syndromes in the light of an evolutionary, systems-immunology model, and suggests that most cytokine amplification conditions… More >
Open Access
ARTICLE
European Cytokine Network, Vol.37, No.1, pp. 25-39, 2026, DOI:10.32604/ecn.2026.077875 - 13 April 2026
Abstract Objectives: B-cell lymphoma exhibits significant clinical heterogeneity, necessitating improved biomarkers for risk stratification. C-C chemokine receptor 7 (CCR7) and trimethylation of histone H3 lysine 9 (H3K9me3) are implicated in cellular senescence and tumor invasion. While the clinical significance of their co-expression in lymphomagenesis remains unclear. This study aims to define the expression profiles of CCR7 and H3K9me3 in B-cell lymphoma, explore their correlation with aggressive clinical indicators, and evaluate their combined prognostic value. Methods: The expression of CCR7 and H3K9me3 in tumor tissues from B-cell lymphoma patients was analyzed by immunohistochemical (IHC) double-staining. The mechanistic… More >