Recent evidence has suggested that signals other than those from Toll-like receptors (TLRs) could contribute to the elicitation of antigen-specific immunity. Therefore, we examined the role of the Nod-like receptor (NLR) family member, Nod1, in the generation of adaptive immune responses. Our findings show that innate immune sensing of peptidoglycan by Nod1 is key for priming antigen-specific T cell immunity and subsequent antibody responses in vivo. Nod1 stimulation alone was sufficient to drive antigen-specific immunity with a predominant Th2 polarization profile. In conjunction with TLR stimulation, however, Nod1 triggering was required to instruct the onset of Th1 and Th2 as well as Th17 immune pathways. Cells outside of the hematopoietic lineage provided the early signals necessary to orchestrate the development of Nod1-dependent immune responses. These findings highlight Nod1 as a key innate immune trigger in the local tissue microenvironment that drives the development of adaptive immunity.
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http://dx.doi.org/10.1016/j.immuni.2007.03.009 | DOI Listing |
EMBO J
January 2025
Philips Institute for Oral Health Research, School of Dentistry, Virginia Commonwealth University, Richmond, VA, USA.
The complement system and neutrophils constitute the two main pillars of the host innate immune defense against infection by bacterial pathogens. Here, we identify T-Mac, a novel virulence factor of the periodontal pathogen Treponema denticola that allows bacteria to evade both defense systems. We show that T-Mac is expressed as a pre-protein that is cleaved into two functional units.
View Article and Find Full Text PDFFish Shellfish Immunol
January 2025
State Key Laboratory of Mariculture Breeding, Key Laboratory of Marine Biotechnology of Fujian Province, Fujian Agriculture and Forestry University, Fuzhou 350002, PR China; University Key Lab for Integrated Chinese Traditional and Western Veterinary Medicine and Animal Healthcare in Fujian Province, Fujian Agriculture and Forestry University, Fuzhou 350002, PR China. Electronic address:
Dietary Astragalus polysaccharides (APS) get wide application in aquaculture due to their excellent immunoregulatory effects. However, little is known about the effects of dietary APS on vaccine potency in fish. In the present study, large yellow croakers (Larimichthys crocea) were injected with formalin-inactivated Pseudomonas plecoglossicida after APS feeding for 14 d and then challenged by live P.
View Article and Find Full Text PDFCell Rep
December 2024
School of Pharmacy, Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem 9112102, Israel; Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA. Electronic address:
Alzheimer's disease (AD) diagnosis relies on the presence of extracellular β-amyloid (Aβ) and intracellular hyperphosphorylated tau (p-tau). Emerging evidence suggests a potential link between AD pathologies and infectious agents, with herpes simplex virus 1 (HSV-1) being a leading candidate. Our investigation, using metagenomics, mass spectrometry, western blotting, and decrowding expansion pathology, detects HSV-1-associated proteins in human brain samples.
View Article and Find Full Text PDFCNS Neurosci Ther
January 2025
Jiujiang Clinical Precision Medicine Research Center, Jiujiang, Jiangxi, China.
Background: Adenosine deaminase action on RNA 1 (ADAR1) can convert the adenosine in double-stranded RNA (dsRNA) molecules into inosine in a process known as A-to-I RNA editing. ADAR1 regulates gene expression output by interacting with RNA and other proteins; plays important roles in development, including growth; and is linked to innate immunity, tumors, and central nervous system (CNS) diseases.
Results: In recent years, the role of ADAR1 in tumors has been widely discussed, but its role in CNS diseases has not been reviewed.
Nat Struct Mol Biol
January 2025
Department of Biological Chemistry, School of Medicine, University of California Irvine, Irvine, CA, USA.
DNA damage in cells induces the expression of inflammatory genes. However, the mechanism by which cells initiate an innate immune response in the presence of DNA lesions blocking transcription remains unknown. Here we find that genotoxic stresses lead to an acute activation of the transcription factor NF-κB through two distinct pathways, each triggered by different types of DNA lesions and coordinated by either ataxia-telangiectasia mutated (ATM) or IRAK1 kinases.
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