
Circulating intercellular adhesion molecule‐1 (ICAM‐1) as an early and sensitive marker for virus‐induced T cell activation
Author(s) -
CHRISTENSEN J. p.,
JOHANSEN J.,
MARKER O.,
THOMSEN A. R.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb03776.x
Subject(s) - lymphocytic choriomeningitis , virus , biology , cd8 , immunology , t cell , mhc class ii , immune system , icam 1 , context (archaeology) , intercellular adhesion molecule 1 , major histocompatibility complex , microbiology and biotechnology , virology , inflammation , cell adhesion molecule , paleontology
SUMMARY The effect of systemic virus infection on the level of circulating ICAM‐1 (cICAM‐1) in serum, and the role of virus‐activated T cells in this context, were studied using the murine lymphocytic choriomeningitis virus infection as primary model system. A marked virus‐induced elevation in cICAM‐1 in serum was revealed, the presence of which coincided with the phase of virus‐induced T cell activation. However, high levels of cICAM‐1 in serum were observed well before maximal T cell activation could be demonstrated. No increase in cICAM‐1 was observed in the serum of infected T cell‐deficient nude mice, clearly demonstrating that T cells were mandatory. Analysis of MHC class I and MHC class II‐deficient mice revealed that either CD4 + or CDS + T cells alone are sufficient, despite a markedly reduced inflammatory exudate in the former animals. These results indicate that virus‐activated T cells induce shedding of ICAM‐1 into the circulation, and this parameter may be used as an early and sensitive marker for immune activation.