title: Targeting Toll-like receptors: emerging therapeutics for multiple sclerosis management.
abstract: 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.
authors: Department of Experimental Pathology and Microbiology, University of Messina, Messina, Italy. gambuzza2002@yahoo.it
authors: M
authors: M
authors: Gambuzza
authors: N
authors: N
authors: Licata
authors: E
authors: E
authors: Palella
authors: D
authors: D
authors: Celi
authors: V
authors: V
authors: Foti Cuzzola
authors: D
authors: D
authors: Italiano
authors: S
authors: S
authors: Marino
authors: P
authors: P
authors: Bramanti
mesh_terms: D000818:Animals; D000529:Complementary Therapies / Q000379:methods / Q000639:trends; D004195:Disease Models, Animal; D006801:Humans; D058990:Molecular Targeted Therapy / Q000379:methods* / Q000639:trends*; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000276:immunology* / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology*; D051193:Toll-Like Receptors / Q000819:agonists / Q000378:metabolism* / Q000502:physiology
chemical_list: D051193:Toll-Like Receptors