Flow cytometric analysis of lymphocytes in cerebrospinal fluid in patients with tick-borne encephalitis

J Tomazic1, A Ihan

  • 1Department of Infectious Diseases, University Medical Centre, Ljubljana, Slovenia.

Insights

Cerebrospinal fluid (CSF) analysis in tick-borne encephalitis (TBE) patients revealed significant differences in lymphocyte subsets compared to peripheral blood. These findings offer insights into the central nervous system

Area of Science:

  • Neuroimmunology
  • Virology
  • Flow Cytometry

Background:

  • Tick-borne encephalitis (TBE) is a viral infection affecting the central nervous system (CNS).
  • Understanding the immune response within the CNS is crucial for TBE pathogenesis.
  • Cerebrospinal fluid (CSF) analysis provides a window into immune cell dynamics during CNS infections.

Purpose of the Study:

  • To quantify and characterize lymphocyte subsets in the CSF of TBE patients.
  • To compare CSF lymphocyte populations with peripheral blood counterparts.
  • To investigate the expression of activation markers on T cells in relation to disease course.

Main Methods:

  • Flow cytometry was used to analyze CSF and peripheral blood samples from 33 TBE patients.
  • Lymphocyte subsets including T cells (CD3+), B cells (CD19+), and NK cells (CD3-CD56+) were quantified.
  • Expression of IL-2 receptors (CD25+), transferrin receptors (CD71+), and HLA-DR molecules on T cells was assessed.

Main Results:

  • T lymphocytes (CD3+) and transferrin receptor-expressing T cells (CD71+) were significantly elevated in CSF compared to peripheral blood.
  • B lymphocytes (CD19+) and NK cells (CD3-CD56+) were more prevalent in peripheral blood.
  • Early TBE infection showed higher HLA-DR expression on T cells, while later stages exhibited increased IL-2 receptor (CD25+) expression.

Conclusions:

  • Significant disparities exist in lymphocyte subset distribution between CSF and peripheral blood in TBE patients.
  • Time-dependent alterations in CSF lymphocyte subsets occur during the course of TBE infection.
  • These findings enhance our understanding of CNS cellular immunopathogenesis in TBE.
Abstract