IgG immunoglobulins induce activation of the sphingomyelin cycle in HL-60 cells.

Abstract:

:In HL-60 cells signal transduction via sphingomyelin hydrolysis (sphingomyelin cycle) is induced by binding of tumor necrosis factor alpha (TNFalpha) to cell surface TNFalpha receptor. We found that IgG immunoglobulins activate sphingomyelin hydrolysis in plasma membrane of HL-60 cells, with kinetics similar to that of activation by TNFalpha. Activation was induced by different IgG isotypes (most of which are irrelevant to known inducers of the sphingomyelin cycle) and also by Fcgamma fragments of IgG. The facts that inhibiting the binding of the antibodies to the cell surface by protein A prevents activation of sphingomyelin hydrolysis and that soluble TNF receptor of 55-kDa subtype (TBP55) inhibits activation, suggest that the mechanism of IgG-induced sphingomyelin hydrolysis involves binding of IgGs through their Fcgamma domain to Fcgamma surface receptors which mediate autocrine secretion of TNFalpha. The latter is responsible for inducing sphingomyelin hydrolysis. This study suggests that TBP55 may be an effective inhibitor of the sphingomyelin cycle.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Glick D,Barenholz Y

doi

10.1016/0014-5793(96)00958-1

subject

Has Abstract

pub_date

1996-10-07 00:00:00

pages

237-40

issue

3

eissn

0014-5793

issn

1873-3468

pii

0014-5793(96)00958-1

journal_volume

394

pub_type

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