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Human β-defensin 2 is involved in CCR2-mediated Nod2 signal transduction, leading to activation of the innate immune response in macrophages

التفاصيل البيبلوغرافية
العنوان: Human β-defensin 2 is involved in CCR2-mediated Nod2 signal transduction, leading to activation of the innate immune response in macrophages
المؤلفون: Ju Kim, Ye Lin Yang, Yong-Suk Jang
المصدر: Immunobiology
سنة النشر: 2019
مصطلحات موضوعية: 0301 basic medicine, CCR2, beta-Defensins, Receptors, CCR2, THP-1 Cells, animal diseases, Immunology, Adaptive immunity, Nod2 Signaling Adaptor Protein, Biology, Article, 03 medical and health sciences, Chemokine receptor, 0302 clinical medicine, Antigen, NOD2, Chlorocebus aethiops, Immunology and Allergy, Animals, Humans, Defensin, Vero Cells, Innate immunity, Innate immune system, Macrophages, hemic and immune systems, Hematology, Macrophage Activation, Acquired immune system, Immunity, Innate, Signaling, Cell biology, Virus, 030104 developmental biology, Host-Pathogen Interactions, Cytokines, Signal transduction, 030215 immunology, Signal Transduction
الوصف: Highlights • HBD 2 enhanced the innate antiviral immune response, including type I IFN induction. • This enhancement was mediated by CCR2-involved and Nod2-mediated signaling. • HBD 2 induced the activation and M1 polarization of macrophage-like THP-1 cells.
Beta-defensins contribute to host innate defense against various pathogens, including viruses, although the details of their roles in innate immune cells are unclear. We previously reported that human β-defensin 2 (HBD 2) activates primary innate immunity against viral infection and suggested that it plays a role in the induction of the adaptive immune response. We analyzed the mechanisms by which HBD 2 primes innate antiviral immunity and polarized activation of macrophage-like THP-1 cells using the receptor-binding domain (RBD) of Middle East respiratory syndrome coronavirus (MERS-CoV) spike protein (S RBD) as a model antigen. The expression of nucleotide-binding oligomerization domain containing 2 (Nod2), type I interferons, (IFNs), and proinflammatory mediators was enhanced in S RBD-HBD 2-treated THP-1 cells. S RBD-HBD 2 treatment also enhanced phosphorylation and activation of receptor-interacting serine/threonine-protein kinase 2 and IFN regulatory factor 3 compared to S RBD alone. Finally, HBD 2-conjugated S RBD interacted with C-C chemokine receptor 2 (CCR2), and Nod2 was involved in HBD 2-mediated CCR2 signaling, which was associated with the activation and M1 polarization of THP-1 cells. Therefore, HBD 2 promotes CCR2-mediated Nod2 signaling, which induces production of type I IFNs and an inflammatory response, and enhances primary innate immunity leading to an effective adaptive immune response to HBD 2-conjugated antigen.
تدمد: 1878-3279
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b9c198008cc89c55b4f8ac832365cd19
https://pubmed.ncbi.nlm.nih.gov/31126693
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....b9c198008cc89c55b4f8ac832365cd19
قاعدة البيانات: OpenAIRE
الوصف
تدمد:18783279