We are analyzing https://link.springer.com/article/10.1007/s00018-024-05191-6.

Title:
cGAS-STING pathway mediates activation of dendritic cell sensing of immunogenic tumors | Cellular and Molecular Life Sciences
Description:
Type I interferons (IFN-I) play pivotal roles in tumor therapy for three decades, underscoring the critical importance of maintaining the integrity of the IFN-1 signaling pathway in radiotherapy, chemotherapy, targeted therapy, and immunotherapy. However, the specific mechanism by which IFN-I contributes to these therapies, particularly in terms of activating dendritic cells (DCs), remains unclear. Based on recent studies, aberrant DNA in the cytoplasm activates the cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling pathway, which in turn produces IFN-I, which is essential for antiviral and anticancer immunity. Notably, STING can also enhance anticancer immunity by promoting autophagy, inflammation, and glycolysis in an IFN-I-independent manner. These research advancements contribute to our comprehension of the distinctions between IFN-I drugs and STING agonists in the context of oncology therapy and shed light on the challenges involved in developing STING agonist drugs. Thus, we aimed to summarize the novel mechanisms underlying cGAS-STING-IFN-I signal activation in DC-mediated antigen presentation and its role in the cancer immune cycle in this review.
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Keywords {🔍}

pubmed, article, google, scholar, cells, cas, sting, cell, cancer, tumor, immune, central, dcs, ifni, activation, dendritic, pathway, cgassting, antitumor, responses, immunity, expression, antigen, human, immunol, agonists, pdcs, type, signaling, tumors, dna, development, response, cdcs, immunotherapy, treatment, therapy, antigens, mice, clinical, nat, role, crosspresentation, tlr, studies, autophagy, mechanisms, activate, ads, ifnα,

Topics {✒️}

antibody-cd20-interferon-alpha fusion protein tumour-induced dendritic-cell defects mediate ifn-i-independent responses ifn-alpha2a induces ip-10/cxcl10 cyclic gmp-amp synthase-stimulator antibody-ifn-β fusion proteins batf3-dependent antigen-presenting cells nf-κb-mediated inflammatory pathway article download pdf rab22a mediates sting-induced nf-κb-induced inflammatory functions cell-mediated tumor-specific cytotoxicity macrophage-dendritic cell progenitors ifn-i-deficient cancer cells sting-s365a mutant mice including ifn-i-independent autophagy mediate contact-dependent killing anti-bdca2 antibody litifilimab monocyte-derived dendritic cells lung-draining lymph nodes ifn-α enhances cross-presentation ifn-i-independent manner tumor-draining lymph nodes cyclic gmp-amp synthase long-lasting cross-presentation enhanced complement-dependent cytotoxicity mechanisms underlying cgas-sting-ifn robust immune-activating properties anti-cd137 mab therapy er-golgi intermediate compart cytosolic dna sensor bolstering antigen cross-presentation ifn-i-independent mechanisms t-mp-based vaccines [154] inosine-mixed cyclic dinucleotides dc-mediated antigen presentation anti-angiogenic properties play enhanced ifn-beta preparations interferon-beta bridges innate ifn-i-mediated activation ifn-induced engulfment receptor sting-mediated antitumor effects cgas/sting cross-talks cisplatin-induced immune modulation retinoic acid-inducible gene lysosome-dependent cell death infection-induced th1 responses potent antigen-presenting cells superior antigen cross-presentation anti-tumor immune function

Questions {❓}

Cancel JC, Crozat K, Dalod M et al (2019) Are conventional type 1 dendritic cells critical for protective antitumor immunity and how?
Nierkens S, Tel J, Janssen E et al (2013) Antigen cross-presentation by dendritic cell subsets: one general or all sergeants?

Schema {🗺️}

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         description:Type I interferons (IFN-I) play pivotal roles in tumor therapy for three decades, underscoring the critical importance of maintaining the integrity of the IFN-1 signaling pathway in radiotherapy, chemotherapy, targeted therapy, and immunotherapy. However, the specific mechanism by which IFN-I contributes to these therapies, particularly in terms of activating dendritic cells (DCs), remains unclear. Based on recent studies, aberrant DNA in the cytoplasm activates the cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling pathway, which in turn produces IFN-I, which is essential for antiviral and anticancer immunity. Notably, STING can also enhance anticancer immunity by promoting autophagy, inflammation, and glycolysis in an IFN-I-independent manner. These research advancements contribute to our comprehension of the distinctions between IFN-I drugs and STING agonists in the context of oncology therapy and shed light on the challenges involved in developing STING agonist drugs. Thus, we aimed to summarize the novel mechanisms underlying cGAS-STING-IFN-I signal activation in DC-mediated antigen presentation and its role in the cancer immune cycle in this review.
         datePublished:2024-03-21T00:00:00Z
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      headline:cGAS-STING pathway mediates activation of dendritic cell sensing of immunogenic tumors
      description:Type I interferons (IFN-I) play pivotal roles in tumor therapy for three decades, underscoring the critical importance of maintaining the integrity of the IFN-1 signaling pathway in radiotherapy, chemotherapy, targeted therapy, and immunotherapy. However, the specific mechanism by which IFN-I contributes to these therapies, particularly in terms of activating dendritic cells (DCs), remains unclear. Based on recent studies, aberrant DNA in the cytoplasm activates the cyclic GMP-AMP synthase (cGAS)- stimulator of interferon genes (STING) signaling pathway, which in turn produces IFN-I, which is essential for antiviral and anticancer immunity. Notably, STING can also enhance anticancer immunity by promoting autophagy, inflammation, and glycolysis in an IFN-I-independent manner. These research advancements contribute to our comprehension of the distinctions between IFN-I drugs and STING agonists in the context of oncology therapy and shed light on the challenges involved in developing STING agonist drugs. Thus, we aimed to summarize the novel mechanisms underlying cGAS-STING-IFN-I signal activation in DC-mediated antigen presentation and its role in the cancer immune cycle in this review.
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      dateModified:2024-03-21T00:00:00Z
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         Type I interferon
         DC
         Tumor immune cycle
         Cell Biology
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         general
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         Biochemistry
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      name:Fujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University, Fuzhou, China
      name:Fujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University, Fuzhou, China
      name:Fujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University, Fuzhou, China
      name:Fujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University, Fuzhou, China
      name:Fujian Key Laboratory of Innate Immune Biology, Biomedical Research Center of South China, College of Life Science, Fujian Normal University, Fuzhou, China

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