Immune molecule found to kill indirectly by closing receptor to live-saving help

Instead of killing damaged cells directly as once believed, an immune molecule works behind the scenes, shutting down receptors within neurons that normally welcome a separate life-saving protein with open arms, a team of scientists says.

The discovery, reported in the Aug. 17 issue of the Proceedings of the National Academy of Sciences, sheds new insight on the cross-talk of two proteins-- insulin-like growth factor, a life-promoting molecule, and an inflammatory cytokine known as tumor necrosis factor alpha (TNF)-- within damaged cells. The findings could become important in the treatment of brain injuries and of Alzheimer's, stroke, multiple sclerosis and AIDS dementia, all of which involve neurodegeneration.

The brains of animals with these injuries and diseases have been injected with large amounts of IGF-I, a pharmaceutical replica of natural growth hormone produced by the liver, to encourage the healing of damaged cells. But, for unexplained reasons, results have not been 100 percent positive.

"Our findings are about life and death and survival of damaged neurons," said Keith W. Kelley, an animal scientist at the University of Illinois and president of the PsychoNeuroImmunology Research Society ( http://www.pnirs.org ).

"Previously, it was believed that IGF and TNF acted completely separately, with IGF inducing life and survival, and TNF simply killing cells directly. Instead TNF is more effective by killing neurons indirectly by scrambling the signal so IGF cannot bind to target cells and produce a survival enzyme", said Homer D. Venters, a student in the M.D.-Ph.D. medical scholars program in the U. of I. College of Medicine at Urbana-Champaign.

The team's findings are based on in vitro experiments with neurons cultured from normal mice. In mammals, IGF induces muscle protein synthesis, enhancing growth and weight gain, except in the pr

Contact: Jim Barlow, Life Sciences Editor
University of Illinois at Urbana-Champaign

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