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Filename: controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
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Function: _error_handler
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Filename: models/Detail_model.php
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Plasmacytoid dendritic cells (pDCs) are a specialized subset of DCs capable of rapidly producing copious amounts of type I IFN (IFN-I) in response to viral infections. The mechanism regulating rapid production of IFN-I after pDCs are exposed to viral nucleic acids remains elusive. Here, we show that the transcription factor Blimp-1 is promptly induced in pDCs after exposure to TLR7 and TLR9 ligands a unique Ras-related C3 botulinum toxin substrate (Rac)-mediated pathway. Deletion of the gene encoding Blimp-1 impaired production of IFN-I, but not other cytokines, upon viral infection or treatment with CpG DNA in pDCs. Accordingly, mice lacking Blimp-1 in DCs failed to produce IFN-I after CpG stimulation and did not mount proper antiviral responses following flavivirus infection. The development of pDCs in bone marrow as well as the induction of several activation markers, such as CD86, CD69, and MHCII, by CpG stimulation was generally not affected by the absence of Blimp-1. Mechanistically, we found that Blimp-1 controls the activation of IKKα and IRF7 by directly suppressing (), a negative regulator of TLR signaling, in pDCs. Together, we identify a Blimp-1-dependent pathway that rapidly facilitates IFN-I production by relieving interleukin-1 receptor-associated kinase M, encoded by , in pDCs.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6091234 | PMC |
http://dx.doi.org/10.3389/fimmu.2018.01828 | DOI Listing |
Fish Shellfish Immunol
December 2024
Department of Marine Life Sciences & Center for Genomic Selection in Korean Aquaculture, Jeju National University, Jeju 63243, Republic of Korea; Marine Life Research Institute, Gidang Marine Research Institute, Jeju National University, Jeju 63333, Republic of Korea. Electronic address:
Tumor necrosis factor-alpha (TNF-α) is a pleiotropic cytokine with critical roles in inflammation, cell survival, and defense. As a member of the TNF superfamily, it exerts its effects by binding to transmembrane receptors and triggering various downstream signaling pathways. Although TNF-α's involvement in antiviral responses in mammals is well-established, its role in teleost remains poorly understood.
View Article and Find Full Text PDFChemMedChem
December 2024
China Pharmaceutical University, State Key Laboratory of Natural Medicines, CHINA.
The activation of the STING-mediated signaling pathway leads to the secretion of type I interferon (IFN) and the activation of tumor-specific T cells. STING, a pattern recognition receptor located on the endoplasmic reticulum membrane of immune cells, binds with endogenous cyclic dinucleotides. STING undergoes phosphorylation, triggering the STING-TBK1-IRF3 pathway and NF-κB pathway, resulting in the release of IFN-β and other pro-inflammatory cytokines, ultimately enhancing the activation of tumor-specific T cells.
View Article and Find Full Text PDFSquamous cell carcinomas (SCC) are often preceded by potentially malignant precursor lesions, most of which remain benign. The terminal exhaustion phenotypes of effector T-cells and the accumulation of myeloid-derived suppressor cells (MDSC) have been thoroughly characterized in established SCC. However, it is unclear what precancerous lesions harbor a bona fide high risk for malignant transformation and how precancerous epithelial dysplasia drives the immune system to the point of no return.
View Article and Find Full Text PDFACS Nano
December 2024
Key Laboratory of Biomedical Polymers of Ministry of Education and Department of Chemistry, Wuhan University, Wuhan 430072, P. R. China.
The blood-brain barrier (BBB) and the immunosuppressive microenvironment of glioblastoma (GBM) severely hinder the infiltration and activity of natural killer (NK) cells, thereby reducing their clinical efficacy in GBM treatment. To address this challenge, we introduced an engineered living material, HEFDS-NK cells, designed to enhance the penetration of NK cells across the BBB and improve their cytotoxicity against GBM. HEFDS comprises magnetic nanoparticles modified using cationic polyethylenimine (PEI), selenocysteine (Sec), and sodium hyaluronate (HA) and cocultured with NK cells to form HEFDS-NK cells.
View Article and Find Full Text PDFArthritis Rheumatol
December 2024
Department of Medicine, University of Cambridge, Cambridge University Hospitals NHS FT, Cambridge, U.K.
Objective: Genetic associations and blockade of the interleukin-23/IL-17 axis with monoclonal antibodies support a role for this pathway in psoriatic arthritis (PsA). This study examines the requirement of IL-23 for IL-17 production, and the role of the metabolic microenvironment in the expansion of Th-derived cells in PsA.
Methods: PsA patient synovial fluid or peripheral blood Th cell frequencies were evaluated by flow cytometry using CCR6, CD161 and T-bet as phenotypic markers, and the cytokines IFN-γ, GM-CSF and IL-17 assessed by flow cytometry and ELISA.
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