Related Experiment Video
Updated: Jul 14, 2026

Assessing the Expression of Major Histocompatibility Complex Class I on Primary Murine Hippocampal Neurons by Flow Cytometry
Published on: May 19, 2020
Distinct regulation of MHC molecule expression on astrocytes and microglia during viral encephalomyelitis
Ludwig Hamo1, Stephen A Stohlman, Maya Otto-Duessel
1Department of Neuroscience, University of Southern California Keck School of Medicine, Los Angeles, California, USA.
Abstract:
The potential interplay of glial cells with T cells during viral induced inflammation was assessed by comparing major histocompatibility complex molecule upregulation and retention on astrocytes and microglia. Transgenic mice expressing green fluorescent protein under control of the astrocyte-specific glial fibrillary acidic protein promoter were infected with a neurotropic coronavirus to facilitate phenotypic characterization of astrocytes and microglia using flow cytometry. Astrocytes in the adult central nervous system up-regulated class I surface expression, albeit delayed compared with microglia. Class II was barely detectable on astrocytes, in contrast to potent up-regulation on microglia. Maximal MHC expression in both glial cell types correlated with IFN-gamma levels and lymphocyte accumulation. Despite a decline of IFN-gamma concomitant to virus clearance, MHC molecule expression on glia was sustained. These data demonstrate distinct regulation of both class I and class II expression by microglia and astrocytes in vivo following viral induced inflammation. Furthermore, prolonged MHC expression subsequent to viral clearance implies a potential for ongoing presentation.
Insights
Glial cells like astrocytes and microglia show distinct major histocompatibility complex (MHC) molecule responses during viral brain inflammation. Their prolonged MHC expression after viral clearance suggests ongoing immune signaling.
Area of Science:
- Neuroimmunology
- Cellular Immunology
- Virology
Background:
- Viral infections trigger neuroinflammation involving glial cells and T cells.
- Major histocompatibility complex (MHC) molecules are crucial for immune cell communication.
- Understanding glial cell responses to viral encephalitis is vital for therapeutic strategies.
Purpose of the Study:
- To investigate the interplay between glial cells (astrocytes and microglia) and T cells during viral-induced central nervous system (CNS) inflammation.
- To compare the expression patterns of MHC class I and class II molecules on astrocytes and microglia in response to viral infection.
Main Methods:
- Utilized transgenic mice expressing green fluorescent protein in astrocytes.
- Infected mice with a neurotropic coronavirus.
- Employed flow cytometry for phenotypic characterization of astrocytes and microglia.
- Quantified MHC molecule expression and correlated it with interferon-gamma (IFN-γ) levels and lymphocyte infiltration.
Main Results:
- Astrocytes upregulated MHC class I expression with a delay compared to microglia.
- Microglia showed potent upregulation of MHC class II, while astrocytes had minimal expression.
- Maximal MHC expression in both cell types correlated with IFN-γ levels and lymphocyte presence.
- MHC molecule expression on glia remained elevated even after IFN-γ levels declined and the virus was cleared.
Conclusions:
- Astrocytes and microglia exhibit distinct regulation of MHC class I and class II expression during viral CNS inflammation.
- Sustained MHC expression on glial cells post-viral clearance indicates a potential for continued antigen presentation.
- These findings highlight the complex role of glial cells in the adaptive immune response within the CNS.
More Related Videos
08:49Simultaneous Isolation of Principal Central Nervous System-Resident Cell Types from Adult Autoimmune Encephalomyelitis Mice
Published on: October 6, 2023
09:38Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
Published on: September 12, 2016
Related Concept Videos
Encephalitis ll: Pathophysiology
Encephalitis l: Introduction