Theiler's virus-infected L-selectin-deficient mice have decreased infiltration of CD8+ T lymphocytes in central nervous system but clear the virus

被引:3
作者
Zhang, XX
Brewer, L
Walcheck, B
Johnson, A
Pease, LR
Njenga, MK
机构
[1] Univ Minnesota, Dept Vet Pathobiol, St Paul, MN 55108 USA
[2] Mayo Clin & Mayo Fdn, Dept Immunol, Rochester, MN 55905 USA
关键词
L-selectin; Theiler's virus; central nervous system; lymphocytes; demyelination;
D O I
10.1016/S0165-5728(01)00296-X
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Mice with targeted deletion of L-selectin gene (L-sel(-/-)) were used to investigate the role of adhesion molecule in immunologic responses following virus infection in the central nervous system (CNS). L-Sel(-/-) mice from a resistant H-2(b) genetic background and parental wild-type H-2(b) (C57BL/6) mice were infected with Theiler's murine encephalomyelitis virus (TMEV) intracerebrally and the kinetics of virus replication and infiltration of immune cells in the CNS determined. The levels of infectious TMEV, as measured by plaque assay at 3, 7, 14, and 28 days after infection were between 4 and 6 log(10) to PFU of virus per gram of CNS tissues at days 3 and 7 post-infection, and then decreased to undetectable levels by day 14 after infection in both strains of mice. The L-sel(-/-) mice had decreased numbers of CD8(+) T lymphocytes (17.72% +/- 2.4) infiltrating into the CNS at 7 days post-infection when compared to wild-type mice (31.02% +/- 7.5). In addition, the L-sel(-/-) mice had significantly lower levels of TMEV-specific serum IgG resulting in lower virus neutralizing activity of the serum when compared to wild-type mice. However, the L-sel(-/-) mice had 2.5-fold increase in B lymphocytes in the CNS (8.29% +/- 1.1) when compared to wild-type mice (3.2% +/- 0.4). Taken together, these data indicate that L-selectin plays a role in recruitment of B and CD8(+) T lymphocytes into the CNS following virus infection, which, however, did not affect the ability of the mice to clear TMEV infection. (C) 2001 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:178 / 187
页数:10
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