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Tumor necrosis factor receptor 2 activation elicits sex-specific effects on cortical myelin proteins and functional recovery in a model of multiple sclerosis
Journal article   Open access   Peer reviewed

Tumor necrosis factor receptor 2 activation elicits sex-specific effects on cortical myelin proteins and functional recovery in a model of multiple sclerosis

Kayla L Nguyen, Ishaan J Bhatt, Shruti Gupta, Nazaf Showkat, Kathryn A Swanson, Roman Fischer, Roland E Kontermann, Klaus Pfizenmaier, Valerie Bracchi-Ricard and John R Bethea
Brain research bulletin, v 207, p110885
Feb 2024
PMID: 38246200
url
https://doi.org/10.1016/j.brainresbull.2024.110885View
Published, Version of Record (VoR) Open

Abstract

tumor necrosis factor (TNF) Multiple sclerosis (MS) experimental autoimmune encephalomyelitis (EAE) TNF receptor 2 (TNFR2) sex differences
Multiple sclerosis (MS), a demyelinating autoimmune disease of the central nervous system (CNS), predominately affects females compared to males. Tumor necrosis factor (TNF), a pro-inflammatory cytokine, signaling through TNF receptor 1 contributes to inflammatory disease pathogenesis. In contrast, TNF receptor 2 signaling is neuroprotective. Current anti-TNF MS therapies are shown to be detrimental to patients due to pleiotropic effects on both pro- and anti-inflammatory functions. Using a non-pertussis toxin (nPTX) experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice, we systemically administered a TNFR2 agonist (p53-sc-mTNF ) to investigate behavioral and pathophysiological changes in both female and male mice. Our data shows that TNFR2 activation alleviates motor and sensory symptoms in females. However, in males, the agonist only alleviates sensory symptoms and not motor. nPTX EAE induction in TNFR2 global knockout mice caused exacerbated motor symptoms in females along with an earlier day of onset, but not in males. Our data demonstrates that TNFR2 agonist efficacy is sex-specific for alleviation of motor symptoms, however, it effectively reduces mechanical hypersensitivity in both females and males. Altogether, these data support the therapeutic promise TNFR2 agonism holds as an MS therapeutic and, more broadly, to treat central neuropathic pain.

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Neurosciences
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