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IFN-α-driven CCL2 production recruits inflammatory monocytes to infection site in mice

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TLDR
CCL2 expression driven by IFI-16 recognition of HSV-1 facilitates the recruitment of inflammatory monocytes into the cornea proper to control viral replication.
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This article is published in Mucosal Immunology.The article was published on 2013-01-01 and is currently open access. It has received 82 citations till now. The article focuses on the topics: Chemokine & Viral replication.

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Journal ArticleDOI

The regulation of inflammation by interferons and their STATs

TL;DR: The goal of this review is to give an overview of the different facets of the inflammatory process that show regulatory input by IFN/STAT.
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Alveolar macrophage–derived type I interferons orchestrate innate immunity to RSV through recruitment of antiviral monocytes

TL;DR: It is demonstrated that this role for recruited inflammatory monocytes in antiviral immunity and protection from RSV infection in mice is critically dependent on the production of type I IFNs by alveolar macrophages triggered via RIG-I–like receptors, thus highlighting an important cell-extrinsic mechanism oftype I IFN–mediated antiviral activity.
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Dynamic control of type I IFN signalling by an integrated network of negative regulators

TL;DR: Evidence is reviewed for an integrated network of negative regulators of IFN production and action, which function at all levels of the activating and effector signalling pathways, to limit tissue damage while enabling an IFN response that is temporally appropriate and of sufficient magnitude.
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Global virus outbreaks: Interferons as 1st responders

TL;DR: Given the direct antiviral effects of type I interferons (IFNs) in inhibiting the replication of both DNA and RNA viruses at different stages of their replicative cycles, and the effects oftype I IFNs on activating immune cell populations to clear virus infections, IFNs-α/β present as ideal candidate broad-spectrum antivirals.
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Phenolic Glycolipid Facilitates Mycobacterial Escape from Microbicidal Tissue-Resident Macrophages

TL;DR: A critical role for mycobacterial membrane phenolic glycolipid (PGL) in engineering this transition to lung alveolar macrophages is defined, arguing for the potential of PGL-blocking interventions or P GL-targeting vaccine strategies in the prevention of tuberculosis.
References
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Journal ArticleDOI

CCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis

TL;DR: The mechanistic link between CCL2 expression and macrophage infiltration are correlated with poor prognosis and metastatic disease in human breast cancer and the origin of these macrophages is defined by showing that Gr1-positive inflammatory monocytes are preferentially recruited to pulmonary metastases but not to primary mammary tumours in mice.
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Targeted Disruption of the MyD88 Gene Results in Loss of IL-1- and IL-18-Mediated Function

TL;DR: It is demonstrated that MyD88 is a critical component in the signaling cascade that is mediated by IL-1 receptor as well as IL-18 receptor, and increases in interferon-gamma production and natural killer cell activity in response to IL- 18 are abrogated.
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Inhibition of viral replication by interferon-gamma-induced nitric oxide synthase

TL;DR: Induction of NO synthase can be necessary and sufficient for a substantial antiviral effect of IFN-gamma and converted resolving ectromelia virus infection into fulminant mousepox in mice.
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Absence of Monocyte Chemoattractant Protein 1 in Mice Leads to Decreased Local Macrophage Recruitment and Antigen-Specific T Helper Cell Type 1 Immune Response in Experimental Autoimmune Encephalomyelitis

TL;DR: It is demonstrated that MCP-1 is crucial for Th1 immune responses in EAE induction and that macrophage recruitment to the inflamed CNS target organ is required for primed T cells to execute a Th1 effector program in Eae.
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