Cited by 42Spinal Cord Injury ResearchNeuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury and Neurovascular Disturbances

Differential Expression of MHC Class II Antigen in the Contused Rat Spinal Cord

POPOVICH, PHILLIP G., STREIT, WOLFGANG J., STOKES, BRADFORD T.·1993·Journal of Neurotrauma

Abstract

Following contusion injury to the dorsal surface of thoracic rat spinal cord, major histocompatibility complex (MHC) class II (Ia) antigen expression by microglia was evaluated throughout the developing lesion. Past investigations of various central nervous system (CNS) lesions have examined short-term or acute sequelae of post-traumatic Ia expression. This report demonstrates that in animals allowed to recover for 18 (sub-chronic) and 45 (chronic) days post-injury, MHC class II antigen is expressed differently at rostral and caudal extents of the lesion as compared with the lesion's epicenter. Following contusion injury to the thoracic spinal cord, sub-chronically injured animals demonstrated Ia-positive microglial staining throughout the white matter rostral and caudal to the epicenter of the lesion, whereas Ia-positive microglia and/or perivascular cells are localized within the gray matter adjacent to it. MHC class II immunoreactivity is down-regulated on microglia at chronic survival times but clusters of Ia-positive macrophages are prominent in regions of maximal degeneration at the epicenter of the lesion. Our findings support the theory that two distinct populations of macrophages participate in resolving traumatic injury. One population is the parenchymal CNS microglia and the other is presumably exudate macrophages derived from the blood. Furthermore, the immunocompetence of these cells as measured by MHC expression may be differentially regulated. This hypothesis is based on differences in Ia-positive staining observed between microglia and macrophages over time concomitant with differences in the spatial distribution of these cell types.

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Registry

Crossref · 10.1089/neu.1993.10.37

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  • Immediately after injury the spinal cord undergoes massive cellular and molecular changes, including increased cell death, infiltration of inflammation cells, axon degeneration, and OL and myelin loss.

    “Immediately after injury the spinal cord undergoes massive cellular and molecular changes, including increased cell death [64, 65], infiltration of inflammation cells in the lesion [2–6], axon degeneration [7–10], and OL and myelin loss [13–16, 66, 67].”

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Authors
POPOVICH, P. G., STREIT, W. J., & STOKES, B. T.
Affiliations
The Ohio State University (US)
Venue
Journal of Neurotrauma
Published
1993-01
Volume
10
Issue
1
Pages
37-46
ISSN
  • 0897-7151 (ISSN-L)
  • 1557-9042
OpenAlex
W2038966835
Cited by
42
References
36
Citations by year
2026: 1 · 2024: 1 · 2023: 1 · 2020: 1 · 2019: 1 · 2015: 3 · 2014: 3
FWCI
1.10
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurotrauma (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p50ns010165-25)
  • National Institute of Neurological Disorders and Stroke (NS-10165)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Keywords
MHC class II antigens, Ia antigens, spinal cord contusion, microglia, macrophages, perivascular cells, traumatic spinal cord injury, thoracic spinal cord, white matter, gray matter, immunocompetence
MeSH terms
Animals, Histocompatibility Antigens Class II, Contusions, Female, Immunohistochemistry, Indicators and Reagents, Neuroglia, Spinal Cord Injuries, T-Lymphocytes, Down-Regulation, Rats, Sprague-Dawley, Rats

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