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Engagement of the Lewis X antigen (CD15) results in monocyte activation
SK Lo, DT Golenbock, PM Sass, A Maskati, H Xu and RL Silverstein
Department of Medicine, Cornell University Medical College, New York, NY
10021, USA.
We previously reported that monocyte adhesion to tumor necrosis factor-
alpha (TNF-alpha)-treated endothelial cells increased expression of tissue
factor and CD36 on monocytes. Using immunological cross-linking to mimic
receptor engagement by natural ligands, we now show that CD15 (Lewis X), a
monocyte counter-receptor for endothelial selectins may participate in this
response. We used cytokine production as a readout for monocyte activation
and found that CD15 cross-linking induced TNF- alpha release from
peripheral blood monocytes and cells from the monocytic cell line MM6.
Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR)
showed an increase in steady-state TNF-alpha mRNA after 3 to 4 hours of
cross-linking. CD15 cross-linking also concomitantly increased
interleukin-1 beta (IL-1 beta) mRNA, while no apparent change was observed
in the levels of beta-actin mRNA, indicating specificity. To examine
transcriptional regulation of cytokine genes by CD15 engagement, a CAT
plasmid reporter construct containing IL-1 beta promoter/enhancer sequences
was introduced into MM6. Subsequent cross-linking of CD15 increased CAT
activity. CD15 engagement by monoclonal antibody also attenuated IL-1 beta
transcript degradation, demonstrating that signaling via CD15 also had
posttranscriptional effects. Nuclear extracts of anti-CD15 cross-linked
cells demonstrated enhanced levels of the transcriptional factor activator
protein-1, minimally changed nuclear factor-kappa B, and did not affect
SV40 promoter specific protein-1. We conclude that engagement of CD15 on
monocytes results in monocyte activation. In addition to its
well-recognized adhesive role, CD15 may function as an important signaling
molecule capable of initiating proinflammatory events in monocytes that
come into contact with activated endothelium.
Volume 89,
Issue 1,
pp. 307-314,
01/01/1997
Copyright © 1997 by The American Society of Hematology
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