作者: Robert N. Lausch , James T. Rector , John E. Oakes
DOI:
关键词: Herpes simplex virus 、 Biology 、 Adoptive cell transfer 、 Viral encephalitis 、 Virus 、 Immune system 、 Immunology 、 Antibody 、 T lymphocyte 、 Virology 、 T cell
摘要: Herpes simplex virus type 1 (HSV-1) inoculated on the abrased cornea of 4-week-old irradiated (450 R) SJL/J mice spread to brain and produced a fatal viral encephalitis by 10-12 days post-infection. Adoptive transfer 2-3 X 10 7 virus-sensitized non-adherent spleen cells 24 hrs before challenge led recovery from infection. Recovery was due suppression HSV-1 replication in rather than prevention central nervous system. If immune were treated with monoclonal anti-Thy 1.2 complement protective effect lost. Pretreatment antibody Lyt-1 membrane antigen also significantly reduced or completely abrogated effect. In contrast, depletion Lyt-2 bearing resulted less-pronounced not statistically significant loss protection. It further observed that cell reconstituted, challenged had considerably higher serum titers (> 10-fold) unreconstituted controls. The results indicate lymphocytes Thy + , Lyt-23" phenotype play predominant role promoting following corneal Invest Ophthalmol Vis Sci 25:188-194, 1984 Previous studies our laboratory have shown herpes (HSV1) specific inoculation do develop herpetic encephalitis.' Treatment animals antithymocyte prior passive 2 Therefore, we speculated may be slowing within system (CNS) until cellular response could initiated. important T resolving subcutaneous intraperitoneal infections has been extensively documented adoptive experiments, 3 " but subsets ocular infection investigated. complexity lymphocyte stimulation recently become recognized. Three designated Lyt-23 23 identified mice. amplify B-cell responses mediated delayed-type hypersensitivity (DTH) reactions, 8