< Back to previous page

Project

IL-13-overexpressing anti-inflammatory Mφs suppress traumainduced premature immune aging. (R-10597)

Besides obvious locomotor impairments, life expectancy of SCI patients is reduced compared to healthy individuals. Hence, a role for premature aging of certain body systems, including cardiovascular, musculoskeletal and respiratory system, has been suggested. Even though it is widely accepted that the immune system is compromised early in SCI patients and that it declines with age, not much is known about how SCI affects ageing of the immune system. Therefore, we will analyse age-related immune markers in mice/humans at different time points after SCI. Recently, promising strategies have been developed to suppress immune-aging, including the use of pharmacological agents that inhibit excessive microglial proinflammatory cytokine secretion (microglia priming). Previously, we have developed macrophages that overexpress the anti-inflammatory cytokine IL-13 (IL-13Mφs), which increase intraspinal alternatively activated Mφ numbers following transplantation in SCI mice. We hypothesize that these IL-13Mφs suppress trauma-induced premature immune-aging, by creating an anti-inflammatory environment to counterbalance microglia priming and T cell immunosenescence. Following transplantation in mice, we will again analyse age-related immune markers. Finally, to translate the results to the human situation, we will test these findings in an immune cellneuronal co-culture system, derived from human induced pluripotent stem cells.
Date:1 Jan 2020 →  31 Dec 2023
Keywords:IL-13, immunology, spinal cord injury
Disciplines:Neurological and neuromuscular diseases