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Tumor necrosis factor is the major monocyte product that increases
complement receptor expression on mature human neutrophils
M Berger, EM Wetzler and RS Wallis
Department of Pediatrics, Case Western Reserve University School of
Medicine, Rainbow Babies and Childrens Hospital, Cleveland, OH 44106.
Interleukin-1 (IL-1) and other monocyte products have several important
effects on the systemic response to infection in addition to their roles in
lymphocyte stimulation. The present studies were carried out to determine
whether products of stimulated monocytes activated circulating neutrophils
(PMN) to increase expression of receptors for C3b (CR1) and C3bi (CR3),
which are necessary for optimal margination, migration, and phagocytosis.
Supernatants of human mononuclear cells that had been stimulated with
lipopolysaccharide (LPS) or purified protein derivative (PPD) contained
both tumor necrosis factor (TNF) and IL-1 and increased CR1 and CR3
expression on isolated PMNs. Supernatants of unstimulated cultures, media
alone, or LPS or PPD alone had little or no effect. Supernatant effects
were detectable at 1:3,000 final dilution and appeared to have a
characteristic slow time course. These supernatants also caused dose- and
time-dependent secretion of PMN granular constituents, but maximal receptor
expression was accompanied by secretion of less than 10% of the cells'
content of lysozyme and less than 16% of the B12 binding protein.
Immunoadsorption studies showed that the supernatant's activity could be
removed by anti- TNF but not by anti-IL-1. Recombinant IL-1 had no effect
on receptor expression, but recombinant TNF increased CR1 and CR3
expression with kinetics similar to the supernatants. These results thus
indicate that TNF is the major monocyte product that increases CR1 and CR3
expression on mature blood neutrophils. This would result in increased
margination and phagocytic activity and may be an important systemic effect
that would help the host eradicate infection.
Volume 71,
Issue 1,
pp. 151-158,
01/01/1988
Copyright © 1988 by The American Society of Hematology
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