Tumor necrosis factor(alpha) and insulin-like growth factor-I in the brain: is the whole greater than the sum of its parts?
The cytokine tumor necrosis factor(alpha) (TNFalpha) and the hormone insulin-like growth factor-I (IGF-I) have both been shown to regulate inflammatory events in the central nervous system (CNS). This review summarizes the seemingly independent roles of TNFalpha and IGF-I in promoting and inhibiting neurodegenerative diseases. We then offer evidence that the combined effects of IGF-I and TNFalpha on neuronal survival can be vastly different when both receptors are stimulated simultaneously, as is likely to occur in vivo. We propose the framework of a molecular model of hormone-cytokine receptor cross talk in which disparate cell surface receptors share intracellular substrates that regulate neuronal survival.
Venters
H D
HD
Laboratory of Immunophysiology, Department of Animal Sciences, College of Medicine, University of Illinois, 207 Edward R. Madigan Laboratory, 1207 West Gregory Drive, Urbana, IL 61801, USA.
Broussard
S R
SR
Zhou
J H
JH
Bluthé
R M
RM
Freund
G G
GG
Johnson
R W
RW
Dantzer
R
R
Kelley
K W
KW
D000818:Animals; D001921:Brain / Q000276:immunology*; D001927:Brain Diseases / Q000276:immunology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
D014409:Tumor Necrosis Factor-alpha; D007334:Insulin-Like Growth Factor I