IL17A and neurodegenerative disease: In a chronic oxidative environment, the inflammatory response is not self-limiting, leading to the persistence of proinflammatory cytokines, particularly the increase in the Th17 response, which is activated by the effect of ozone [3,8], as well as in response to bacteria and fungi [49], and remains active during the development of autoimmune [50] and neurodegenerative diseases through the secretion of IL17 [51], with a notable decrease in IL-10 [8].