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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
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Functional expression of chemokine receptor CCR5 on CD4(+) T cells during virus-induced central nervous system

William G Glass1, Thomas E Lane

  • 1Department of Molecular Biology and Biochemistry, University of California, Irvine 92697-3900, USA.

Journal of Virology
|December 13, 2002
PubMed

Insights

Chemokine receptor CCR5 is crucial for CD4(+) T cell entry into the central nervous system (CNS) during mouse hepatitis virus (MHV) infection. This migration is essential for clearing the virus and driving demyelination, similar to multiple sclerosis (MS).

Area of Science:

  • Neuroimmunology
  • Virology
  • Immunology

Background:

  • Mouse hepatitis virus (MHV) infection in C57BL/6 mice causes acute encephalomyelitis and demyelination, mimicking human multiple sclerosis (MS).
  • CD4(+) T cells are key players in demyelination by recruiting macrophages to the central nervous system (CNS) post-viral infection.
  • The precise mechanisms controlling CD4(+) T cell entry into the CNS remain inadequately understood.

Purpose of the Study:

  • To investigate the role of chemokine receptor CCR5 in the trafficking of virus-specific CD4(+) T cells into the CNS during MHV infection.
  • To elucidate how CCR5 signaling influences the expression of other chemokine receptors involved in T cell migration.

Main Methods:

  • CD4(+) T cells from CCR5(+/+) and CCR5(-/-) mice were expanded using the MHV M133-147 epitope.
  • Adoptive transfer of these T cells into MHV-infected RAG1(-/-) mice.
  • Analysis of T cell CNS infiltration, viral titers, macrophage accumulation, demyelination, and chemokine receptor mRNA expression.

Main Results:

  • Transfer of CCR5(+/+) CD4(+) T cells led to CNS entry, viral clearance, macrophage accumulation, and demyelination.
  • CCR5(-/-) CD4(+) T cells showed impaired CNS trafficking, resulting in higher viral loads, less macrophage infiltration, and reduced demyelination.
  • CCR5 deficiency correlated with reduced expression of CCR1, CCR2, and CXCR3 on CD4(+) T cells.

Conclusions:

  • CCR5 signaling is essential for the migration of CD4(+) T cells into the CNS following MHV infection.
  • CCR5 plays a critical role in orchestrating the expression of other chemokine receptors necessary for T cell homing to the CNS.
  • These findings highlight CCR5 as a potential therapeutic target for CNS demyelinating diseases like MS.

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