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Related Concept Videos

Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Related Experiment Video

Updated: Nov 30, 2025

Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
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Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation

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Microglial responses to peripheral type 1 interferon.

Ernest Aw1,2, Yingying Zhang1, Michael Carroll3

  • 1Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA.

Journal of Neuroinflammation
|November 13, 2020
PubMed
Summary
This summary is machine-generated.

Peripheral Interferon α (IFNα) directly alters microglia, impacting gene expression and synaptic pruning. This IFNα-induced C4b upregulation may contribute to neuropsychiatric conditions.

Keywords:
ComplementInterferon alpha (IFNα)Interferon-stimulated gene (ISG)MicrogliaNeuropsychiatricSynapse engulfment

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Related Experiment Videos

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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
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Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Interferon α (IFNα) is linked to neuropsychiatric deficits in autoimmune diseases like SLE.
  • Mechanisms of IFNα's CNS effects and its influence on microglia-mediated synaptic pruning are unclear.

Purpose of the Study:

  • Investigate how peripheral IFNα signaling affects microglia gene expression and function.
  • Determine if IFNα directly impacts microglia and influences synaptic pruning.

Main Methods:

  • Administered peripheral IFNα to mice and analyzed gene expression in sorted microglia via bulk RNA sequencing.
  • Assessed microglia morphology and synapse engulfment using immunohistochemistry and flow cytometry.
  • Utilized microglia-specific Ifnar1 conditional knockout mice to confirm direct IFNα signaling effects.

Main Results:

  • IFNα exposure induced a unique microglial gene signature, including interferon-stimulated genes (ISGs) and complement component C4b.
  • Observed IFNα-dependent changes in microglial phenotype (CD45, CD68 expression, morphology, synapse engulfment) with brain region-specific differences.
  • Demonstrated that these changes are primarily due to direct IFNα-IFNAR signaling on microglia.

Conclusions:

  • Peripheral IFNα induces direct genetic and phenotypic changes in microglia via IFNAR signaling.
  • IFNα-induced C4b upregulation in microglia may play a role in aberrant synaptic pruning in neuropsychiatric disorders.