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Related Concept Videos

T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

838
T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
838

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Ovalbumin-specific CD4

Rouven Wannemacher1, Anna Reiß1,2, Karl Rohn3

  • 1Department of Pathology, University of Veterinary Medicine Hannover, Foundation, Hannover, Germany.

Frontiers in Immunology
|June 9, 2023
PubMed
Summary

Theiler's murine encephalomyelitis virus (TMEV) infection in specific mouse models reveals distinct disease mechanisms. OT-I mice showed severe pathology due to high viral load and lack of CD8+ T cells, while OT-II mice exhibited immunopathology driven by CD4+ T cells.

Keywords:
OT miceOVA-specific CD4+ T cellsOVA-specific CD8+ T cellsT cell dependent susceptibilityTheiler’s murine encephalomyelitis virus (TMEV)central nervous systemmicrogliosisneuroimmunology

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Area of Science:

  • * Neuroimmunology
  • * Virology
  • * Demyelinating Diseases

Background:

  • * Theiler's murine encephalomyelitis virus (TMEV) causes TMEV-induced demyelinating disease (TMEV-IDD), a model for multiple sclerosis (MS).
  • * TMEV-IDD pathogenesis involves viral persistence and T cell-mediated immunopathology in susceptible hosts.
  • * OT mice, lacking specific T cell populations on a resistant background, were used to investigate TMEV susceptibility.

Purpose of the Study:

  • * To investigate the role of antigen-specific T cells in TMEV susceptibility and pathogenesis.
  • * To compare disease progression and outcomes in OT-I, OT-II, and control mice after TMEV infection.

Main Methods:

  • * Intracerebral infection of OT-I, OT-II, and C57BL/6 mice with TMEV-BeAn strain.
  • * Weekly clinical scoring, followed by histological and immunohistochemical analysis of the central nervous system (CNS).
  • * Assessment of viral load and immune cell infiltration (CD4+ and CD8+ T cells).

Main Results:

  • * OT-I mice developed severe progressive motor dysfunction, high cerebral viral load, and lacked CNS CD8+ T cells.
  • * OT-II mice showed variable disease severity, with some recovering, correlating with reduced CD8+ T cell infiltration and increased CD4+ T cells in the brain.
  • * TMEV-infected OT-I mice exhibited direct virus-associated pathology, while OT-II mice showed evidence of immunopathology.

Conclusions:

  • * The absence of specific T cell populations influences TMEV susceptibility and disease course.
  • * Distinct mechanisms, including direct viral pathology (OT-I) and immunopathology (OT-II), contribute to TMEV-IDD in these models.
  • * Further research is needed to elucidate the precise pathomechanisms in OT mice following TMEV infection.