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AN INFLUENZA HEMAGGLUTININ-SPECIFIC IGG ENHANCES CLASS-I MHC-RESTRICTED CTL KILLING INVITRO

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UNSPECIFIED (1991) AN INFLUENZA HEMAGGLUTININ-SPECIFIC IGG ENHANCES CLASS-I MHC-RESTRICTED CTL KILLING INVITRO. IMMUNOLOGY, 73 (1). pp. 12-18.

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Abstract

Lungs of H-2k mice co-inoculated with type A/WSN influenza virus + detective interfering WSN virus contain haemagglutinin (HA)-specific IgG which have three different activities. These have been purified by adsorbtion and elution using different forms of HA. The first IgG recognizes HA in a form present on H-2k cells infected with a vaccinia virus recombinant expressing the WSN HA gene (vaccinia-HA virus), but not on virus particles, and enhances class I major histocompatibility complex (MHC)-restricted killing of WSN-infected H-2k target cells by primary cytotoxic T lymphocytes (CTL) from the lungs of WSN-infected H-2k mice; it also confers on primary CTL from the lungs of WSN-infected H-2d mice the ability to lyse WSN-infected H-2k targets. This IgG is therefore analogous to the T-cell receptor in that it is antigen specific and MHC restricted. A second IgG recognizes HA in a form present on both H-2k and H-2d cells infected with the vaccinia-HA virus but not present on virus particles and inhibits CTL lysis of WSN-infected syngeneic target cells. Only the third binds to virus particles; this inhibits agglutination of red cells, but is non-neutralizing. It also inhibits CTL lysis of WSN-infected syngeneic targets. Thus we present evidence that HA-specific IgG may have a significant role in regulating CTL responses to influenza virus in vivo and that one of these IgG is MHC-restricted in its recognition of viral antigen. Finally, in vivo significance of these antibodies is indicated by the finding that adoptively transferred CTL-enhancing IgG protects mice from lethal WSN infection.

Item Type: Journal Article
Subjects: Q Science > QR Microbiology > QR180 Immunology
Journal or Publication Title: IMMUNOLOGY
Publisher: BLACKWELL SCIENCE LTD
ISSN: 0019-2805
Official Date: May 1991
Dates:
DateEvent
May 1991UNSPECIFIED
Volume: 73
Number: 1
Number of Pages: 7
Page Range: pp. 12-18
Publication Status: Published

Data sourced from Thomson Reuters' Web of Knowledge

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