Type I interferon signaling contributes to the development of innate and adaptive immune responses to either viruses, fungi, or bacteria. However, amplitude and timing of the interferon response is of utmost importance for preventing an underwhelming outcome, or tissue damage. While several pathogens evolved strategies for disturbing the quality of interferon signaling, there is growing evidence that this pathway can be regulated by several members of the Nod-like receptor (NLR) family, although the precise mechanism for most of these remains elusive. NLRs consist of a family of about 20 proteins in mammals, which are capable of sensing microbial products as well as endogenous signals related to tissue injury. Here we provide an overview of our current understanding of the function of those NLRs in type I interferon responses with a focus on viral infections. We discuss how NLR-mediated type I interferon regulation can influence the development of auto-immunity and the immune response to infection.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7865845 | PMC |
| http://dx.doi.org/10.3390/ijms22031301 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Early transcriptional effects of inflammatory cytokines reveal highly redundant cytokine networks.
J Exp Med
April 2025
Department of Immunology, Harvard Medical School, Boston, MA, USA.
Inflammatory cytokines are fundamental mediators of the organismal response to injury, infection, or other harmful stimuli. To elucidate the early and mostly direct transcriptional signatures of inflammatory cytokines, we profiled all immunologic cell types by RNAseq after systemic exposure to IL1β, IL6, and TNFα. Our results revealed a significant overlap in the responses, with broad divergence between myeloid and lymphoid cells, but with very few cell-type-specific responses.
View Article and Find Full Text PDFInfectious bursal disease virus affecting interferon regulatory factor 7 signaling through VP3 protein to facilitate viral replication.
Front Cell Infect Microbiol
January 2025
Guangxi Key Laboratory for Polysaccharide Materials and Modifications, School of Marine Sciences and Biotechnology, Guangxi Minzu University, Nanning, Guangxi, China.
Interferon regulatory factor 7 (IRF7)-mediated type I interferon antiviral response is crucial for regulating the host following viral infection in chickens. Infectious bursal disease virus (IBDV) is a double-stranded RNA virus that induces immune suppression and high mortality rates in chickens aged 3-6 weeks. Previous studies have shown that IBDV infection antagonizes the type I interferon production to facilitate viral replication in the cell, and IRF7 signaling might play an important role.
View Article and Find Full Text PDFIncreased interferon I signaling, DNA damage response and evidence of T-cell exhaustion in a patient with combined interferonopathy (Aicardi-Goutières Syndrome, AGS) and cohesinopathy (Cornelia de Lange Syndrome, CdLS).
Pediatr Rheumatol Online J
January 2025
Laboratory of Autoimmunity and Inflammation, Center for Clinical, Biomedical Research Foundation, Experimental Surgery and Translational Research, Academy of Athens, Athens, Greece.
Background: Type I interferonopathies including Aicardi-Goutiéres Syndrome (AGS) represent a heterogeneous group of clinical phenotypes. Herein, we present a Case with combined AGS and Cornelia de Lange Syndrome (CdLS)-a cohesinopathy-with comprehensive analysis of the immune and genomic abnormalities.
Case And Methods: A 20-year old man presented with chilblain lesions and resorption of distal phalanges of fingers and toes, somatic and psychomotor retardation, microcephaly, synophrys, hearing losing and other aberrancies consistent with the phenotype of CdLS.
Assessment and management for latent tuberculosis before advanced therapies for immune-mediated inflammatory diseases: A comprehensive review.
Autoimmun Rev
January 2025
Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Electronic address:
Tuberculosis (TB), caused by Mycobacterium TB, is the most significant infectious cause of mortality across the globe. While TB disease can prey on immunocompetent individuals, it is more likely to occur in immunocompromised individuals. Immune-mediated inflammatory diseases (IMIDs) are a group of diseases (rheumatoid arthritis, inflammatory bowel disease, ankylosing spondylitis, psoriasis, hidradenitis suppurative, autoimmune blistering diseases, and others) where there may be a need for systemic immunosuppression to control the disease manifestations, treat symptoms and improve long term outcomes.
View Article and Find Full Text PDFIdentification and Validation of a m6A-Related Long Noncoding RNA Prognostic Model in Colorectal Cancer.
J Cell Mol Med
January 2025
Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang, China.
Accumulating research indicates that N6-methyladenosine (m6A) modification plays a pivotal role in colorectal cancer (CRC). Hence, investigating the m6A-related long noncoding RNAs (lncRNAs) significantly improves therapeutic strategies and prognostic assessments. This study aimed to develop and validate a prognostic model based on m6A-related lncRNAs to improve the prediction of clinical outcomes and identify potential immunological mechanisms in CRC.
View Article and Find Full Text PDFWant 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!