Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Persistent type I interferon (IFN-I) signaling compromises adaptive anti-HIV-1 T cell immunity and promotes viral reservoir persistence, yet its effects on innate lymphoid cells during chronic infection remain unclear. Through integrated single-cell RNA sequencing and functional validation in HIV-1-infected humanized mice with combination antiretroviral therapy (cART) and IFN-I signaling blockade, we reveal IFN-I-induced dysfunction of natural killer (NK) cells and group 3 innate lymphoid cells (ILC3s). Mechanistically, the IFN-I-CD9 axis drives NK cells toward a decidual NK cell-like phenotype, impairing their cytotoxic activity. Furthermore, IFNAR blockade rescues ILC3 functionality, which is critical for IL-17/IL-22-mediated antimicrobial defense and mucosal barrier maintenance. Our study delineates IFN-I-driven immunosuppression across innate lymphocyte compartments and proposes the targeted modulation of this pathway to enhance antiviral and mucosal immunity in HIV-1 management.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12390710 | PMC |
| http://dx.doi.org/10.3390/v17081099 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Restoration of the lamina propria duodenal immune infiltrate in gluten-free diet treated coeliac patients despite persistent villous atrophy.
Clin Exp Immunol
September 2025
Mucosal Immunology Lab, Department of Paediatrics and Immunology. Universidad de Valladolid. Valladolid. Spain.
Introduction: Although Coeliac disease (CD) current and only treatment is a life-long strict gluten free diet (GFD), some patients suffer from persistent duodenal lesions despite years into the diet. Hence, we aimed to study the effect that the GFD elicits on the mucosal immune infiltrate from these patients.
Method: To that end, duodenal biopsies were collected from non-coeliac controls and CD patients, both at diagnosis and after at least one year into the GFD.
T follicular helper cells (T): From physiological to pathological aging.
Eur J Intern Med
September 2025
Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy; Istituti Clinici Scientifici ICS Maugeri - S.p.A.-Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) Istituto Scientifico di Telese Terme, Telese, Italy. Electronic address:
The fraction that the elderly represent in the world's population is growing rapidly; numerous alterations that impact all organs and systems, including the immune system, are related to aging. A complex process common in the elderly, known as immunosenescence, is characterized by a decreased ability to respond to vaccination as well as an increased risk of bacterial and viral infections, autoimmune, cardiovascular and neurodegenerative diseases. These processes are associated with alterations in the innate and adaptive immune system and lead to a condition of chronic low-grade inflammation, referred to as inflammaging.
View Article and Find Full Text PDFRelationship between CFTR variants, sweat chloride responses, and lung function improvements.
Lancet Respir Med
September 2025
Department for Paediatric Pneumology, Allergology, and Neonatology and German Center for Lung Research, Biomedical Research in Endstage and Obstructive Lung Disease, Hannover Medical School, 30625 Hannover, Germany. Electronic address:
IL-25-induced memory type 2 innate lymphoid cells enforce mucosal immunity.
Cell
September 2025
Department of Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. Electronic address:
Adaptation of intestinal helminths to vertebrates involved the evolution of strategies to attenuate host tissue damage to support parasite reproduction and dissemination of offspring to the environment. Helminths initiate the IL-25-mediated tuft cell-type 2 innate lymphoid cell (ILC2) circuit that enhances barrier protection of the host, although viable parasites can target and limit this pathway. We used IL-25 alone to create small intestinal adaptation, marked by anatomic and immunologic changes that persisted months after induction.
View Article and Find Full Text PDFDDX3X mutation and Epstein-Barr virus cooperate to induce R-loop-dependent oncogenesis.
Cell Rep
September 2025
Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China; Pôle de Recherches Sino-Français en Science du Vivant et Gé
RNA helicase DDX3X is generally implicated in inflammasome activation and anti-viral responses. We characterize the common features of scattered DDX3X mutations in lymphoid cancers using molecular dynamics simulation and crystallization, thereby demonstrating their crucial role in Epstein-Barr virus (EBV) lytic gene-driven oncogenic processes. The DDX3X mutation is significantly related to impaired stimulator of interferon genes (STING)/ interferon regulatory factor 7 (IRF-7)/interferon (IFN)-α/β-mediated innate immunity, overexpression of EBV lytic gene BNLF2b, and increased formation of R-loops.
View Article and Find Full Text PDF