T cell memory specific for self and non-self antigens in rats persistently infected with Borna disease virus.
We have studied CD4+ Th1 T cell responses in Borna disease (BD), a virus-mediated immune disease of the central nervous system (CNS), and demonstrate the priming of virus-specific as well as autoreactive T cells specific for myelin antigens in the course of viral infection. The fate of these in vivo generated T cells was subsequently assessed by in vitro proliferation assays with lymphocytes from different lymphoid organs of diseased animals over a long period of time. Virus-specific T cell responses continuously decreased during the establishment of persistent infection and could no longer be detected after 5-6 months post infectionem, when inflammatory reactions in the brain had ceased. By contrast, autoantigen-specific T cells kept their ability to mount characteristic secondary responses--although at an overall rather low level--over long periods of time; these autoreactive T cells homed to a specific lymphoid organ, the perithymic lymph node. Our study thus describes for the first time a complete decline of virus-specific T cell memory in a persistent viral infection, and raises the question how long-lasting T cell autoreactivity is controlled.
Rott
O
O
Institut für Virologie, Universität Giessen, Germany.
Herzog
S
S
Cash
E
E
D000595:Amino Acid Sequence; D000818:Animals; D001890:Borna Disease / Q000276:immunology*; D003429:Cross Reactions; D005260:Female; D007156:Immunologic Memory; D008969:Molecular Sequence Data; D004676:Myelin Basic Protein / Q000276:immunology; D009185:Myelin Proteins / Q000276:immunology; D018991:Myelin Proteolipid Protein; D051381:Rats; D011917:Rats, Inbred Lew; D013601:T-Lymphocytes / Q000276:immunology*
D004676:Myelin Basic Protein; D009185:Myelin Proteins; D018991:Myelin Proteolipid Protein