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Changes in cell adhesion molecule expression on T cells associated with systemic virus infection
E C Andersson1, J P Christensen, O Marker
1Institute of Medical Microbiology and Immunology, University of Copenhagen, Panum Institute, Denmark.
Journal of Immunology (Baltimore, Md. : 1950)
|February 1, 1994
Summary
Virus infection up-regulates adhesion molecules like VLA-4 on CD8+ T cells, enhancing their migration to inflammatory sites. This study highlights VLA-4
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Understanding T cell migration is crucial for antiviral immunity.
- Adhesion molecules regulate immune cell trafficking.
- Viral infections alter immune cell behavior.
Purpose of the Study:
- To investigate virus-induced changes in T cell adhesion molecule expression.
- To understand the role of these changes in effector T cell migration to infectious foci.
Main Methods:
- Flow cytometry (FACS) analysis of T cells from virus-infected mice.
- Assessment of cell adhesion molecules (VLA-4, LFA-1, ICAM-1) and homing receptors (MEL-14).
- Correlation of adhesion molecule expression with cellular activation markers (IL-2R) and CTL activity.
Main Results:
- Systemic lymphocytic choriomeningitis virus infection up-regulated VLA-4, LFA-1, and ICAM-1 on CD8+ T cells.
- MEL-14 (lymph node homing receptor) was down-regulated on CD8+ T cells.
- Up-regulation of VLA-4 on splenic T cells correlated with inflammatory cell influx into cerebrospinal fluid and increased CD8+VLA-4hi cell counts in blood and CSF.
Conclusions:
- Virus infection alters T cell adhesion molecule profiles, promoting migration to inflammatory sites.
- Up-regulation of VLA-4 is critical for effector T cell homing to sites of inflammation.
- These findings provide insights into immune cell trafficking during viral infections.