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The Gender Gap in Multiple Sclerosis Intersection of Science and Society

Shannon E. Dunn, PhD; Lawrence Steinman, MD
JAMA Neurol. 2013;70(5):634-635. doi:10.1001/jamaneurol.2013.55.
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More than 3 times more women than men have multiple sclerosis (MS). Over the past 50 years, this ratio has been steadily increasing.1,2 The burdens to those who battle this disease, as well as the costs for society in dealing with MS, are substantial, and deciphering this 50-year-old trend in female preponderance in this disease is critical.1,2 In attempting to understand this growing imbalance, a number of intriguing discoveries have been made. These discoveries illuminate the pathogenesis of MS, with applications and benefits for both men and women. These breakthroughs potentially allow for the repurposing of certain approved drugs for potential use as treatments of MS.

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Figure. Model of the regulation of the sexual dimorphism of TH cytokine production by peroxisome proliferator–activated receptor α (PPARα) and PPARγ. A higher androgen level in men in conjunction with T-cell receptor or CD28 signaling enhances PPARα expression in CD4+ T cells. As a result, the brake normally imposed on TH17 by PPARγ (red symbols) is removed (crossed-out red symbols), while PPARα continues to inhibit TH1. Consequently, male T cells are more prone to make the TH17 cytokine IL-17A. Conversely, the lower androgen level in women leads to lowered PPARα expression and enhanced PPARγ expression in activated CD4+ T cells. As a result, the brake on TH1 by PPARα is lifted while the TH17 suppression by PPARγ persists. Consequently, we found female T cells to be more prone to make the TH1 cytokine IFN-γ. The green symbols indicate the mechanisms of cross-inhibition between TH1 and TH17 pathways. The red symbols indicate inhibitory pathways modulated by PPARs.




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