Circulating intercellular adhesion molecule-1 (ICAM-1) as an early and sensitive marker for virus-induced T cell

J P Christensen1, J Johansen, O Marker

  • 1Institute of Medical Microbiology and Immunology, University of Copenhagen, Denmark.

Insights

Systemic viral infections elevate circulating intercellular adhesion molecule-1 (cICAM-1) levels. Virus-activated T cells are essential for this increase, making cICAM-1 a potential early immune activation marker.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Systemic viral infections can trigger significant immune responses.
  • Intercellular adhesion molecule-1 (ICAM-1) plays a role in immune cell adhesion and trafficking.
  • The precise role of T cells in regulating circulating ICAM-1 during viral infections is not fully understood.

Purpose of the Study:

  • To investigate the effect of systemic viral infection on circulating ICAM-1 (cICAM-1) levels.
  • To determine the role of virus-activated T cells in modulating cICAM-1.
  • To assess cICAM-1 as a potential biomarker for immune activation.

Main Methods:

  • Murine lymphocytic choriomeningitis virus (LCMV) infection model.
  • Analysis of serum cICAM-1 levels in wild-type, T cell-deficient (nude), MHC class I, and MHC class II-deficient mice.
  • Monitoring of T cell activation phases during infection.

Main Results:

  • A significant virus-induced elevation in serum cICAM-1 was observed.
  • Elevated cICAM-1 levels preceded maximal T cell activation.
  • T cells were mandatory for the increase in cICAM-1, as evidenced by studies in nude mice.
  • Both CD4+ and CD8+ T cells were sufficient to induce cICAM-1 shedding.

Conclusions:

  • Virus-activated T cells induce the shedding of ICAM-1 into circulation.
  • Serum cICAM-1 serves as an early and sensitive indicator of immune activation during viral infections.
  • This finding has implications for monitoring immune responses in viral pathogenesis.

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