TY - JOUR
T1 - Changes in cell adhesion molecule expression on T cells associated with systemic virus infection
AU - Andersson, E C
AU - Christensen, Jan Pravsgaard
AU - Marker, O
AU - Thomsen, Allan Randrup
N1 - Keywords: Animals; Antigens, CD8; Cell Adhesion Molecules; Cerebrospinal Fluid; Cytotoxicity, Immunologic; Female; Flow Cytometry; Intercellular Adhesion Molecule-1; L-Selectin; Lymphocyte Activation; Lymphocyte Function-Associated Antigen-1; Lymphocytic Choriomeningitis; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Mice, Inbred C57BL; Receptors, Very Late Antigen; T-Lymphocyte Subsets; T-Lymphocytes, Cytotoxic
PY - 1994
Y1 - 1994
N2 - Virus-induced changes in adhesion molecule expression on T cells were investigated to understand how antiviral effector cells migrate into infectious foci. FACS analysis revealed that after systemic infection with lymphocytic choriomeningitis virus a number of cell adhesion molecules, including VLA-4, LFA-1, and ICAM-1, are up-regulated on CD8+ cells, whereas the lymph node homing receptor MEL-14 is down-regulated during the infection; only marginal changes were observed for CD4+ cells. Basically similar but less marked results were obtained in mice infected with Pichinde virus. Further analyses showed that T cells with a changed adhesion molecule profile tended to present other cell surface markers indicating a state of cellular activation, e.g., IL-2R, and included all virus-specific CTL effectors. Regarding the physiologic significance of these changes in adhesion molecule expression, it was found that up-regulation of VLA-4 expression on splenic T cells correlated with influx of inflammatory cells into the cerebrospinal fluid of intracerebrally infected animals, and that the number of CD8+VLA-4hi cells increased from lymph nodes and spleen to blood and cerebrospinal fluid. These results support the hypothesis that up-regulation of VLA-4 is important for effector T cell homing to sites of inflammation.
AB - Virus-induced changes in adhesion molecule expression on T cells were investigated to understand how antiviral effector cells migrate into infectious foci. FACS analysis revealed that after systemic infection with lymphocytic choriomeningitis virus a number of cell adhesion molecules, including VLA-4, LFA-1, and ICAM-1, are up-regulated on CD8+ cells, whereas the lymph node homing receptor MEL-14 is down-regulated during the infection; only marginal changes were observed for CD4+ cells. Basically similar but less marked results were obtained in mice infected with Pichinde virus. Further analyses showed that T cells with a changed adhesion molecule profile tended to present other cell surface markers indicating a state of cellular activation, e.g., IL-2R, and included all virus-specific CTL effectors. Regarding the physiologic significance of these changes in adhesion molecule expression, it was found that up-regulation of VLA-4 expression on splenic T cells correlated with influx of inflammatory cells into the cerebrospinal fluid of intracerebrally infected animals, and that the number of CD8+VLA-4hi cells increased from lymph nodes and spleen to blood and cerebrospinal fluid. These results support the hypothesis that up-regulation of VLA-4 is important for effector T cell homing to sites of inflammation.
M3 - Journal article
C2 - 7507962
VL - 152
SP - 1237
EP - 1245
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 3
ER -