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Journal of Virology, November 1999, p. 9650-9654, Vol. 73, No. 11
Department of Immunology, St. Jude
Children's Research Hospital, Memphis, Tennessee 38105
Received 5 May 1999/Accepted 22 July 1999
Respiratory challenge with the murine gammaherpesvirus 68 (
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Requirement for CD40 Ligand, CD4+ T
Cells, and B Cells in an Infectious Mononucleosis-Like
Syndrome


HV-68) results in productive infection of the lung, the
establishment of latency in B lymphocytes and other cell types,
transient splenomegaly, and prolonged clonal expansion of activated
CD8+ CD62Llo T cells, particularly a
V
4+ CD8+ population that is found in mice
with different major histocompatibility complex (MHC) haplotypes.
Aspects of the CD8+-T-cell response are substantially
modified in mice that lack B cells, CD4+ T cells, or the
CD40 ligand (CD40L). The B-cell-deficient mice show no increase in
V
4+ CD8+ T cells. Similar abrogation of the
V
4+ CD8+ response is seen following
antibody-mediated depletion of the CD4+ subset, through the
numbers of CD8+ CD62Llo cells are still
significantly elevated. Virus-specific CD4+-T-cell
frequencies are minimal in the CD40L
/
mice, and the
V
4+ CD8+ population remains unexpanded.
Apparently B-cell-CD4+-T-cell interactions play a part in
the
HV-68 induction of both splenomegaly and non-MHC-restricted
V
4+ CD8+-T-cell expansion.
*
Corresponding author. Mailing address: Department of
Immunology, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN 38105. Phone: (901) 495-3470. Fax: (901) 495-3107. E-mail:
peter.doherty{at}stjude.org.
Present address: Transduction Laboratories, Inc., Lexington, KY 40511.
Present address: Infectious Diseases, Parke-Davis Pharmaceutical
Research, Ann Arbor, MI 48103.
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