Posted on May 30, 2016, 6 a.m.
Mechanism of aging also plays role in weakening the immune system.
Oxidative stress is a biological process that is emerging as a major factor in both diseases and aging itself. Environmental influences such air pollution, smoking, and UV radiation can release free radicals into the body, submitting it to oxidative stress that can in-turn weaken the immune system. Mai Matsushita, from ETH Zurich's Institute of Molecular Health Sciences (Switzerland), and colleagues have revealed that the immune response fails to work if significant oxidative stress is damaging T-cell immune cells. The investigators employed a mouse model in which they deactivated selenoenzyme glutathione peroxidase 4 (Gpx4) – a major free radical scavenger, to observe that the lack (or defective) Gpx4 caused T cells to die off as they divided, rendering them unable to eliminate the pathogen and permitting infection to become chronic. Observing that: “Ex vivo, Gpx4-deficient T cells rapidly accumulated membrane lipid peroxides and concomitantly underwent cell death driven by ferroptosis but not necroptosis,” the study authors submit that: “ These studies unveil an essential role of Gpx4 for T cell immunity.”
Matsushita M, Freigang S, Schneider C, Conrad M, Bornkamm GW, Kopf M. “T cell lipid peroxidation induces ferroptosis and prevents immunity to infection.” Journal of Experimental Medicine, April 6, 2015; 212(4):555-68.`