Leptin
<p>From: 'Getting “Younger”: Leptin, Chronic Fatigue Syndrome and Fibromyalgia' <a href="https://www.healthrising.org/blog/2015/01/26/getting-younger-leptin-chronic-fatigue-fibromyalgia/">https://www.healthrising.org/blog/2015/01/26/getting-younger-leptin-chronic-fatigue-fibromyalgia/</a></p>
<p>From: TheEmergingRoleofAutoimmunityinMyalgicEncephalomyelitisChronicFatigueSyndromeME</p>
<p>Leptin levels are elevated by prolonged activation of proinflammatory cytokines [190] and subsequently have profound effects on the immune system further predisposing to an autoimmune environment. Leptin exerts a stimulatory effect on NO production [191] and further upregulates the activity of proinflammatory cytokines [183, 192]. Elevated levels of leptin potentiate the production of IL-12, IFN-γ, and IL-2 and suppress the synthesis of IL-10 and IL-4 [193, 194]. Activated T cell survival and proliferation are both enhanced by leptin [195, 196], while the proliferation of FOXP3 CD4 + CD25+ Tregs is inhibited by this cytokine [183]. Evidence suggests that elevated levels of leptin leads to the activation and improved survival of resting T and B lymphocytes with subsequent secretion of TNF-α and IL-6 by both cell types [197]. Leptin also modulates the secretion of pro-inflammatory cytokines and chemokines by macrophages [193], monocytes [198], and eosinophils [199]. Dendritic cell survival and Th1 priming are both increased by elevated leptin levels as is their production of proinflammatory and Th1 cytokines [200]. All in all, elevated levels of leptin may induce a de novo autoimmune environment by inducing the activation of T and B cells while driving T cell differentiation towards the Th1 or Th17 phenotype or by potentiating the deleterious effects of an already chronically activated immune system. In the forthcoming final section, we consider the management role of B cells and their contribution to autoimmune pathology which exists quite independently of their ability to produce antibodies. </p>