Author: Evans, Claire F.; Horwitz, Marc S.; Hobbs, Monte V.; Oldstone, Michael B.A.
Title: Viral Infection of Transgenic Mice Expressing a Viral Protein in Oligodendrocytes Leads to Chronic Central Nervous System Autoimmune Disease Document date: 1996_12_1
ID: t82a9y5s_28
Snippet: To address whether infection of LCMV-immune mice with VV or PV reactivated LCMV-specific CTL as has been observed in C57BL/6 mice (33), BALB/c mice were infected with LCMV; after 6 wk they were given a second viral infection with VV or PV. In addition, these viruses were also injected into BALB/c mice that had not received the initial LCMV infection. At 5-7 d after infection, splenic lymphocytes were isolated and tested in an in vitro 51 Cr-relea.....
Document: To address whether infection of LCMV-immune mice with VV or PV reactivated LCMV-specific CTL as has been observed in C57BL/6 mice (33), BALB/c mice were infected with LCMV; after 6 wk they were given a second viral infection with VV or PV. In addition, these viruses were also injected into BALB/c mice that had not received the initial LCMV infection. At 5-7 d after infection, splenic lymphocytes were isolated and tested in an in vitro 51 Cr-release assay for LCMV-specific CTL activity. Although primary VV-or PV-specific CTL did not recognize LCMV-infected target cells, infection of LCMV-immune BALB/c mice with either virus resulted in the activation of LCMV-specific CTL memory cells capable of lysing MHCmatched (Table 2) but not mismatched (data not shown) LCMV-infected target cells. This indicated that infection of LCMV-immune mice with a second virus not encoding LCMV gene products activated LCMV-specific CTL.
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