As we age, the immune system gradually becomes impaired. One aspect of thisA Balancing Act Between Immunity and Longevity; Mutation in Splicing Factor RNP-6 Inhibits Immune Response in C. elegans, But Increases Lifespan, Barring Infection; RNP-6 Human Orthologue Splicing Factor PUF60 May Also Be Involved in Immunity & Lifespan impairment is chronic inflammation in the elderly, which means that the immune system is constantly active and sends out inflammatory substances. Such chronic inflammation is associated with multiple age-related diseases including arthritis and Alzheimer's disease, and impaired immune responses to infection. One of the questions in aging research is whether chronic inflammation is a cause of aging, or a consequence of the aging process itself? Scientists in the laboratory of Adam Antebi, PhD, Director of the Max Planck Institute for Biology of Aging in Cologne, Germany, have found evidence suggesting that increased inflammation causes the aging process to speed up, and that there is a fine balance between maintaining immune system function and longevity. From their work in the tiny roundworm, Caenorhabditis elegans, the scientists discovered a mutation in an evolutionarily conserved gene [the RNP-6 (ribonucleoprotein 6) gene in C. elegans, whose orthologous gene in humans is called PUF60 (poly U binding splicing factor 60)], which made the worms long-lived, but, at the same time, dampened their immune response. Worms with this mutation lived about 20% longer than normal worms, but when they were infected with certain bacteria, they succumbed more quickly to the infection. This suggests that an overactive immune system also has a price: it shortens life span. Conversely, a less active immune system pays off in a longer life span--as long as the animal does not die from an infection.
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