MOUSE PARVOVIRUS INFECTION POTENTIATES ALLOGENEIC SKIN-GRAFT REJECTION AND INDUCES SYNGENEIC GRAFT-REJECTION

Citation
M. Mckisic et al., MOUSE PARVOVIRUS INFECTION POTENTIATES ALLOGENEIC SKIN-GRAFT REJECTION AND INDUCES SYNGENEIC GRAFT-REJECTION, Transplantation, 65(11), 1998, pp. 1436-1446
Citations number
68
Categorie Soggetti
Transplantation,Surgery,Immunology
Journal title
ISSN journal
00411337
Volume
65
Issue
11
Year of publication
1998
Pages
1436 - 1446
Database
ISI
SICI code
0041-1337(1998)65:11<1436:MPIPAS>2.0.ZU;2-A
Abstract
Background. The recently identified autonomous mouse parvovirus design ated mouse parvovirus-1 (MPV-1) persists in adult BALB/c mice for at l east 9 weeks, infects lymphoid tissues, interferes with the ability of cloned T cells to proliferate, and exhibits immunomodulatory properti es. As a consequence of these findings, the present studies were under taken to characterize further the immunomodulatory effects of MPV-1 on T cell-mediated immune responses in vivo and in vitro. Methods. To ev aluate the effect of MPV-1 infection on CD8(+) T cell-mediated respons es, BALB/c-H2(dm2) mice were infected after transplantation of allogen eic BALB/c skin. Results. MPV-1 potentiated the rejection of allogenei c skin grafts. This potentiation was not a result of virus infecting t he cellular or vascular component of the graft as determined by in sit u hybridization, but was mediated by T cells. However, the proliferati ve capacity of alloantigen-reactive lymphocytes from graft-sensitized infected mice was diminished. MPV-1 also induced the rejection of syng eneic skin grafts, and T cells from these infected graft-sensitized mi ce lysed syngeneic P815 target cells. Conclusions. These results sugge st that MPV-1 infection of skin-grafted mice may disrupt normal mechan isms of peripheral tolerance and provide a unique model to study virus -induced autoimmunity.