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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1362-1369
Migration of activated CD8+ T lymphocytes to sites of
viral infection does not require endothelial selectins
Christina Bartholdy,
Ole Marker, and
Allan Randrup Thomsen
From the Institute of Medical Microbiology and Immunology,
University of Copenhagen, Denmark.
Using mice deficient of E-selectin and E/P-selectin, we have studied
the requirement for endothelial selectins in extravasation of
leukocytes at sites of viral infection, with major emphasis on the
recruitment of virus-specific TC1 cells. Lymphocytic
choriomeningitis virus (LCMV)-induced meningitis was used as
our primary experimental model. Additionally, localized subdermal
inflammation and virus clearance in internal organs were analyzed
during LCMV infection. The generation of CD8+ effector T
cells in infected mutants was unimpaired. Quantitative and qualitative
analysis of the inflammatory exudate cells in intracerebrally infected
mice gave identical results in all strains of mice. Expression of
endothelial selectin was also found to be redundant regarding the
ability of effector cells to eliminate virus in nonlymphoid organs.
Concerning LCMV-induced footpad swelling, absent or marginal reduction
was found in E/P-sel  / mice, compared with wild-type mice after
local challenge with virus or immunodominant viral MHC class I
restricted peptide, respectively. Similar results were obtained after
adoptive transfer of wild-type effector cells into E/P-sel /
recipients, whereas footpad swelling was markedly decreased in
P-sel/ICAM-1 / and ICAM-1 / recipients. LCMV-induced footpad swelling was completely inhibited in ICAM-deficient mice transfused with donor cell preincubated with soluble VCAM-1-Ig chimeric
protein. Taken together, the current findings strongly indicate that
the migration of TC1 effector cells to sites of viral
infection can proceed in the absence of endothelial selectins, whereas
ligands of the Ig superfamily are critically involved in this process.
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