The effect of hydrocortisone (HC) on in vitro human polymorphonuclear leukocyte cytotoxicity was studied. HC was able to inhibit reversibly and in a dose-dependent way the antibody-dependent cellular cytotoxicity (ADCC) and the phytohemagglutinin-dependent cellular cytotoxicity (PDCC). The killing defect was partially overcome by increasing the antibody or the phytohemagglutinin (PHA) concentrations on the target cells. HC inhibited the PDCC more efficiently than ADCC; in fact the inhibition was present even at 10-5 M HC levels. Higher concentrations caused a progressive reduction in both tests. Inhibition of these PMN-mediated cytotoxicities may explain, in part, bot the anti-inflammatory actions of steroids and their deleterious effects on host defenses.

Inhibition of polymorphonuclear leukocyte-mediated cytotoxicity by hydrocortisone "in vitro" / F. Capsoni, P. L. Meroni, M. R. Zocchi, A. Plebani. - In: BOLLETTINO DELL'ISTITUTO SIEROTERAPICO MILANESE. - ISSN 0021-2547. - 60:2(1981 May), pp. 113-120.

Inhibition of polymorphonuclear leukocyte-mediated cytotoxicity by hydrocortisone "in vitro"

F. Capsoni
Primo
;
P. L. Meroni
Secondo
;
1981-05

Abstract

The effect of hydrocortisone (HC) on in vitro human polymorphonuclear leukocyte cytotoxicity was studied. HC was able to inhibit reversibly and in a dose-dependent way the antibody-dependent cellular cytotoxicity (ADCC) and the phytohemagglutinin-dependent cellular cytotoxicity (PDCC). The killing defect was partially overcome by increasing the antibody or the phytohemagglutinin (PHA) concentrations on the target cells. HC inhibited the PDCC more efficiently than ADCC; in fact the inhibition was present even at 10-5 M HC levels. Higher concentrations caused a progressive reduction in both tests. Inhibition of these PMN-mediated cytotoxicities may explain, in part, bot the anti-inflammatory actions of steroids and their deleterious effects on host defenses.
Cytotoxicity, Immunologic; Antibody-Dependent Cell Cytotoxicity; Hydrocortisone; Neutrophils; Phytohemagglutinins; Humans
Settore MED/16 - Reumatologia
http://www.ncbi.nlm.nih.gov/pubmed/7306390
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/194723
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