Abstract:
:We have investigated if recombinant granulocyte-macrophage colony stimulating factor (GM-CSF), alone or in concert with recombinant gamma interferon, affects the endothelial cell expression of class I major histocompatibility complex antigen. Results obtained show that the GM-CSF increases class I expression on the endothelial cell in a time- and dose-dependent manner. The effect of interferon gamma on class I expression is diminished in the presence of GM-CSF, cAMP, or prostaglandin E2, but is increased in the presence of cGMP. N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA 1004), an inhibitor of cAMP- and cGMP-dependent protein kinases, abolished GM-CSF-induced class I expression, while indomethacin increased it. When added to the endothelial cell cultures together with interferon gamma GM-CSF, HA 1004 as well as indomethacin abolished the inhibitory effect of GM-CSF on interferon gamma-induced class I expression. The results suggest that GM-CSF diminishes effect of interferon gamma on class I major histocompatibility complex expression on the endothelial cell by inducing production of rostacyclin. This, in turn, induces cAMP as a second messenger, which then leads to the events inhibiting expression of class I major histocompatibility complex antigen.
journal_name
Hum Immunoljournal_title
Human immunologyauthors
Leszczynski D,Häyry Pdoi
10.1016/0198-8859(90)90016-isubject
Has Abstractpub_date
1990-06-01 00:00:00pages
175-8issue
2eissn
0198-8859issn
1879-1166pii
0198-8859(90)90016-Ijournal_volume
28pub_type
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