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  • Book
    Contents:
    1. [Symposia I-III]
    2. [Symposia IV-VII]
    3. Colloquia I-XIV
    4. General sessions A-F
    5. General sessions G-J
    [6] Author index
    [7] Supplement I-
    Print Access Request
    Location
    Version
    Call Number
    Items
    Stored offsite. Please request print.
    v. 1, 3-6, Supp. 1, 1967.
    F501 .I61a 1967
    6
  • Article
    Doherty PC, Biddison WE, Bennink JR, Knowles BB.
    J Exp Med. 1978 Aug 01;148(2):534-43.
    Secondary effector T-cell populations generated by cross-priming with heterologous influenza A viruses operate only in H-2K or H-2D compatible situations, when assayed on SV40-transformed target cells infected with a range of influenza A viruses. The H2-Kb allele is associated with a total failure in the generation of influenza-immune cytotoxic T cells, though this is not seen for the primary response to vaccinia virus. In both influenza and vaccinia development of effector T cells operating at H-2Db is greatly depressed in B10.A(2R) (kkkddb) and B10.A(4R) (kkbbbb), but not in B10 (bbbbbb), mice. However, there is no defect in viral antigen expression at either H-2Kk or H-2Db in B10.A(2R) target cells. This apparently reflects some inadequacy in the stimulator environment, as (A/J X B6) F1 T cells can be induced to respond at H-2Db when exposed to vaccinia virus in an irradiated B6 but not in a B10.A(4R) recipient. The present report, together with the accompanying paper by Zinkernagel and colleagues, records the first rigorous demonstration of both a nonresponder situation and a probable Ir-gene effect for conventional infectious viruses. Possible implications for the evolution of H-2 polymorphism and mechanisms of Ir gene function are discussed.
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