International Immunology, Vol 10, 791-797, Copyright © 1998 by Oxford University Press
X Yu, R Abe and RJ Hodes
The role of B7 co-stimulatory signaling in in vivo tumor rejection remains
incompletely characterized. In particular, the relative competence of B7-1
(CD80) and B7-2 (CD86) to provide effective co- stimulus is not well
defined, and the identification of the T cell co- stimulatory receptor that
mediates B7 co-stimulation in tumor rejection has not been addressed. These
issues were studied by assessing rejection of B7-negative or B7-transfected
tumor cells in CD28- expressing or CD28-deficient hosts. B7-negative EL4
tumor cells grew progressively in normal syngeneic C57BUL6 (B6) mice. In
contrast EL4 cells transfected with either full length B7-1 or full length
B7-2 were rejected, indicating that both B7-1 and B7-2 are competent to
mediate rejection of EL4 tumor cells. Expression of truncated B7-1 or B7-2
products, with complete deletion of cytoplasmic domains, was as effective
as expression of full length B7-1 or B7-2 in mediating rejection. In
contrast to the rejection of B7-transfected EL4 cells observed in
CD28-expressing syngeneic hosts, B7-1- and B7-2-positive EL4 cells as well
as control EL4 cells grew progressively in CD28- deficient mice,
demonstrating the requirement for host expression of CD28 in B7-mediated
tumor rejection. These results indicate that interaction of host CD28 with
co-stimulatory extracellular B7-1 or B7-2 ligands expressed on tumor cells
can play a necessary role in mediating tumor rejection.
ARTICLES
The role of B7-CD28 co-stimulation in tumor rejection
Experimental Immunology Branch, National Cancer Institute and National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA.
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