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Journal of Virology, January 2000, p. 203-208, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
B7 Costimulation Is Critical for Antibody Class
Switching and CD8+ Cytotoxic T-Lymphocyte Generation in the
Host Response to Vesicular Stomatitis Virus
Alexander J.
McAdam,1,*
Evan A.
Farkash,2
Benjamin E.
Gewurz,1 and
Arlene H.
Sharpe1
Departments of Pathology, Brigham and
Women's Hospital and Harvard Medical
School1 and Harvard
University,2 Boston, Massachusetts 02115
Received 30 July 1999/Accepted 27 September 1999
Antibody and cytotoxic T-lymphocyte (CTL) responses have critical
roles in eliminating many viral infections. In addition to stimulation
of the T-cell receptor, T cells require costimulatory signals to
respond optimally. We evaluated the role of B7 costimulatory molecules
(B7-1 and B7-2) in the immune response to viral infection using
vesicular stomatitis virus (VSV) and mice lacking either B7-1 or B7-2
or both molecules. Mice lacking both B7-1 and B7-2 had essentially no
anti-VSV immunoglobulin G1 (IgG1) response, decreased IgG2a responses,
and normal IgM responses, while mice lacking either B7-1 or B7-2 had
unaltered anti-VSV antibody responses compared to wild-type mice.
Depletion of CD4+ cells further reduced the IgG2a response
in mice lacking both B7 molecules, suggesting that CD4
cells may supply help for IgG2a in the absence of B7 costimulation. The
absence of both B7 molecules profoundly reduced generation of both
primary and secondary VSV-specific class I major histocompatibility complex (MHC)-restricted CTL, whereas VSV-specific CTL responses in
mice lacking either B7-1 or B7-2 were similar to those of wild-type animals. Class I MHC-restricted CTL in wild-type mice were not dependent on CD4+ cells, suggesting that the failure of CTL
in the absence of B7s is due to a lack of B7 costimulation directly to
the CD8+ CTL. These data demonstrate that B7-1 and B7-2
have critical, overlapping functions in the antibody and CTL responses
to this viral infection.
*
Corresponding author. Mailing address: Department of
Pathology, LMRC 5th floor, 221 Longwood Ave., Boston, MA 02115. Phone: (617) 278-0317. Fax: (617) 732-5795. E-mail:
ajmcadam{at}bics.bwh.harvard.edu.
Journal of Virology, January 2000, p. 203-208, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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