Title : Potential role of resident islet macrophage activation in the initiation of autoimmune diabetes.

Pub. Date : 1998 Mar 15

PMID : 9510167






4 Functional Relationships(s)
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Compound Name
Protein Name
Organism
1 The IL-1R antagonist protein completely prevents TNF + LPS-induced nitrite production, iNOS expression and the inhibitory effects on glucose-stimulated insulin secretion by rat islets. Nitrites tumor necrosis factor Rattus norvegicus
2 IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. Nitrites tumor necrosis factor Rattus norvegicus
3 IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. Nitrites tumor necrosis factor Rattus norvegicus
4 IL-1beta appears to mediate the inhibitory actions of TNF + LPS on beta cell function as TNF + LPS-induced expression of IL-1beta is fourfold higher than IL-1alpha, and Ab neutralization of IL-1beta prevents TNF + LPS-induced nitrite production by rat islets. Nitrites tumor necrosis factor Rattus norvegicus