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Lymphocytic Choriomeningitis Virus Infection is Associated with Long‐Standing Perturbation of LFA‐1 Expression on CD8 + T Cells
Author(s) -
ANDERSSON E. C.,
CHRISTENSEN J. PRAVSGAARD,
SCHEYNIUS A.,
MARKER O.,
THOMSEN A. RANDRUP
Publication year - 1995
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1995.tb03633.x
Subject(s) - lymphocytic choriomeningitis , biology , cytotoxic t cell , cd8 , population , lymphocyte function associated antigen 1 , immunology , microbiology and biotechnology , cell adhesion molecule , antigen , intercellular adhesion molecule 1 , medicine , biochemistry , environmental health , in vitro
Flow cytometric analysis of splenocytes from mice infected with lymphocytic Choriomeningitis virus revealed marked and long‐standing up‐regulation of LFA‐1 expression on CD8 + , but not on CD4 + T cells. Appearance of CD8 + T cells with a changed expression of adhesion molecules reflected polyclonal activation and expansion which was demonstrated not to depend on CD4 + T cells or their products. Cell sorting experiments defined virus‐specific CTL to be included in this population (LFA‐1 hi MEL‐14 lo ), but since about 80% of splenic CD8 + T cells have a changed phenotype, extensive bystander activation must take place; this is indicated also by the finding that CD8 + LFA‐l hi cells transiently express several markers of cellular activation, e. g. transferrin receptor, IL‐2Rα and β. Analysis of cells from the cerebrospinal fluid of mice infected intracerebrally showed that virtually all T cells present belonged to the CD8LFA‐l hi subset and, correspondingly, the ligand ICAM‐1 was found to be up‐regulated on endothelial cells in the inflamed meninges. Preincubation of LCMV‐primed donor splenocytes with anti‐LFA‐1 markedly inhibited the transfer of virus‐specific delayed‐type hypersensitivity to naive recipients. Together, these findings indicate that up‐regulation of LFA‐1 expression is a critical factor involved in directing activated CD8 + T cells to sites of viral infection.