Abstract
Leukocytes rapidly lose their surface receptors for TNF and IL-1 upon exposure to various stimuli in vitro. We sought to determine by FACS analysis changes in the expression of TNF receptors (TNFR) and type II IL-1R on circulating monocytes and granulocytes during endotoxemia in vivo, and the role of endogenous TNF in these changes. Twelve healthy subjects received an i.v. injection with LPS (2 ng/kg), directly preceded by a 30-min infusion of either a recombinant human dimeric TNFR type II-IgG fusion protein (TNFR:Fc; 6 mg/m2; n = 6) or vehicle (n = 6). LPS administration was associated with decreases in the expression of types I and II TNFR and type II IL-1R on both monocytes and granulocytes. Treatment with TNFR:Fc completely neutralized LPS-induced TNF activity (p <0.0001 vs LPS only), modestly blunted the decrease in monocyte TNFR (p <0.05), but did not influence reduced expression of granulocyte TNFR or monocyte/granulocyte type II IL-1R. In separate experiments, rTNF added to whole blood reduced cellular type I and type II TNFR expression by an effect on the type I TNFR; TNF did not (monocytes) decrease or only marginally (granulocytes) decreased type II IL-1R expression. LPS induces down-modulation of monocyte and granulocyte receptors for TNF and IL-1 in humans in vivo. TNF is involved in reduced monocyte TNFR expression during endotoxemia
Original language | Undefined/Unknown |
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Pages (from-to) | 1490-1497 |
Journal | The journal of immunology |
Volume | 158 |
Issue number | 3 |
Publication status | Published - 1997 |
Keywords
- AMC wi-eigen