ArticlebioRxiv : the preprint server for biology2025
Beta Adrenergic Signaling as a Therapeutic Target for Autoimmunity.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: We recently identified a molecular mechanism involving beta-adrenergic 1 and 2 receptors (β1/2) in the development of T Methods: Multiple sclerosis (MS) is an inflammatory demyelinating disorder of the central nervous system (CNS) characterized by an autoimmune response where both T-lymphocytes and IL-17A are implicated in the pathogenesis of the disease. Using an animal model of MS, termed experimental autoimmune encephalomyelitis (EAE), we addressed the impact of beta adrenergic receptor blockade (genetically and pharmacologically) on EAE disease progression, severity, and T Results: The genetic deletion β1/2 receptors, either systemically or specifically in T-lymphocytes, significantly attenuated EAE disease severity and animal weight loss. Pharmacological blockade of β1/2 receptors with either propranolol (lipophilic) or nadolol (aqueous) limited disease severity and weight loss similar to the genetic models. All models showed degrees of shifted T Conclusions: Our data depict a novel role for β1/2 adrenergic signaling in the control of T
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