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• W1964107900 abstract "<h2>Abstract</h2> Toll-like receptors (TLR) are important innate immune proteins for the identification and clearance of invading pathogen. TLR signal through adaptor proteins, most commonly myeloid differentiation primary response gene 88 (MyD88). Inappropriate response of specific TLR has been implicated in certain autoimmune diseases, such as multiple sclerosis (MS). Activation of TLR2, TLR4, TLR7 and TLR9 plays a role in experimental allergic encephalomyelitis (EAE), a murine model of MS, while TLR3 activation protects from disease. Therefore, TLR-modulation could be an important adjuvant to current treatments. Here, we focus on TLR involved in EAE and MS pathogenesis highlighting specific components targeting TLR that might offer further therapeutic possibilities." @default.
• W1964107900 created "2016-06-24" @default.
• W1964107900 creator A5012901664 @default.
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• W1964107900 creator A5090129180 @default.
• W1964107900 date "2011-10-01" @default.
• W1964107900 modified "2023-09-29" @default.
• W1964107900 title "Targeting Toll-like receptors: Emerging therapeutics for multiple sclerosis management" @default.
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