Document 0091
 DOCN  M9580091
 TI    Alpha 4 integrin directs virus-activated CD8+ T cells to sites of
       infection.
 DT    9506
 AU    Christensen JP; Andersson EC; Scheynius A; Marker O; Thomsen AR;
       Institute of Medical Microbiology, University of Copenhagen,; Denmark.
 SO    J Immunol. 1995 May 15;154(10):5293-301. Unique Identifier : AIDSLINE
       MED/95248095
 AB    This article examines the role of VLA-4 in directing lymphocytes to
       sites of viral infection using the murine lymphocytic choriomeningitis
       virus infection (LCMV) as the model system. This virus by itself induces
       little or no inflammation, but in most mouse/virus strain combinations a
       potent T cell response is induced, which is associated with marked CD8+
       cell-mediated inflammation. Two expressions of LCMV-induced inflammation
       were studied: meningitis induced by intracerebral infection and adoptive
       transfer of virus-specific delayed-type hypersensitivity. Our previous
       studies have shown that LCMV infection results in the appearance of
       activated CD8+ cells with an increased expression of VLA-4. In this
       study we have compared various T cell high and low responder situations,
       and these experiments revealed that acute inflammation correlates
       directly with VLA-4 expression on splenic CD8+ cells. This correlation
       could be extended to CD4+ and B cells in chronically infected low
       responder DBA/2 mice. The vascular ligand for VLA-4, VCAM-1, was found
       to be up-regulated on endothelial cells in sites of inflammation.
       Finally, preincubation of virus-primed donor cells with mAb to VLA-4
       completely blocked the ability to transfer virus-specific, delayed-type
       hypersensitivity when the donor cells were given i.v., but not when the
       cells were injected directly into the test site. Co-transfer of
       CD8-depleted cells with anti-VLA-4-blocked cells did not reveal any
       cooperation. Taken together, these results indicate that VLA-4 play a
       critical role in lymphocyte homing during systemic virus infections and
       are involved in directing virus-specific CD8+ effector cells to sites of
       infection.
 DE    Animal  Antibodies, Monoclonal/IMMUNOLOGY  Cell Adhesion
       Molecules/BIOSYNTHESIS/IMMUNOLOGY  Cell Movement/IMMUNOLOGY
       Cytotoxicity Tests, Immunologic  CD8-Positive T-Lymphocytes/*IMMUNOLOGY
       Endothelium, Vascular/IMMUNOLOGY  Female  Flow Cytometry
       Hypersensitivity, Delayed/IMMUNOLOGY  Immunoenzyme Techniques
       Immunotherapy, Adoptive  Lymphocytic
       Choriomeningitis/*IMMUNOLOGY/MORTALITY  Mice  Mice, Inbred BALB C  Mice,
       Inbred C3H  Mice, Inbred DBA  Receptors, Very Late
       Antigen/BIOSYNTHESIS/*IMMUNOLOGY  Support, Non-U.S. Gov't  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).