Inflammation 2004,
PMID: 15527169
Eslick, Joy; Scatizzi, John C; Albee, Lee; Bickel, Emily; Bradley, Kathleen; Perlman, Harris
Human peripheral blood monocytes undergo spontaneous apoptosis in culture. Spontaneous monocyte apoptosis is regulated by the death ligand, Fas Ligand (FasL) binding to its receptor Fas. The pro-inflammatory molecules, LPS and IL-1beta, prevent spontaneous monocyte apoptosis. Here, we demonstrate that the anti-inflammatory cytokines IL-4 and IL-10 inhibit spontaneous monocyte apoptosis compared to control-treated cells. IL-4- or IL-10-mediated suppression of spontaneous monocyte apoptosis is associated with the induction of Flip, an essential inhibitor of the Fas-death signal. In contrast, IL-4 and IL-10 inhibit LPS or IL-1beta induced pro-inflammatory cytokine production. These data suggest that in monocytes IL-4 or IL-10 has a dual function, to inhibit pro-inflammatory cytokine production and to suppress spontaneous apoptosis.
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Text Mining Data
IL-1beta ⊣ IL-10: "
In contrast, IL-4 and
IL-10 inhibit LPS or
IL-1beta induced pro-inflammatory cytokine production
"
IL-1beta ⊣ IL-4: "
In contrast, IL-4 and IL-10 inhibit LPS or IL-1beta induced pro-inflammatory cytokine production
"
LPS ⊣ IL-10: "
In contrast, IL-4 and IL-10 inhibit LPS or IL-1beta induced pro-inflammatory cytokine production
"
LPS ⊣ IL-4: "
In contrast, IL-4 and IL-10 inhibit LPS or IL-1beta induced pro-inflammatory cytokine production
"
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