
The recognition of viral components by host pattern-recognition receptors triggers the induction of the antiviral innate immune response. Toll-like receptor 9 (TLR9) and NLRP3 inflammasome were shown to be the principal specific sensors of viral double-stranded DNA. Here we present evidence that macrophages in vivo activated an innate immune response to a double-stranded DNA virus, adenovirus (Ad), independently of TLR9 or NLRP3 inflammasome. In response to Ad, macrophage-derived IL-1 alpha triggered IL-1RI-dependent production of a defined set of proinflammatory cytokines and chemokines. The IL-1 alpha-mediated response required a selective interaction of virus arginine-glycine-aspartic acid (RGD) motifs with macrophage beta(3) integrins. Thus, these data identify IL-1 alpha-IL-1RI as a key pathway allowing for the activation of proinflammatory responses to the virus, independently of its genomic nucleic acid recognition.
Mice, Knockout, MICROBIO, Macrophages, Immunology, Genetic Vectors, Integrin beta3, Receptors, Interleukin-1, Immunity, Innate, Adenoviridae, Mice, Inbred C57BL, Mice, Infectious Diseases, CELLIMMUNO, Interleukin-1alpha, Toll-Like Receptor 9, NLR Family, Pyrin Domain-Containing 3 Protein, Immunology and Allergy, Animals, MOLIMMUNO, Carrier Proteins, Spleen
Mice, Knockout, MICROBIO, Macrophages, Immunology, Genetic Vectors, Integrin beta3, Receptors, Interleukin-1, Immunity, Innate, Adenoviridae, Mice, Inbred C57BL, Mice, Infectious Diseases, CELLIMMUNO, Interleukin-1alpha, Toll-Like Receptor 9, NLR Family, Pyrin Domain-Containing 3 Protein, Immunology and Allergy, Animals, MOLIMMUNO, Carrier Proteins, Spleen
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| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 1% |
