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Am J Clin Exp Immunol 2013;2(1):75-93
Review Article
Role of toll-like receptors in multiple sclerosis
Socorro Miranda-Hernandez, Alan G Baxter
Comparative Genomics Centre, Molecular Sciences Building 21, James Cook University, Townsville, QLD 4811, Australia
Received December 12, 2012; Accepted January 16, 2013; Epub February 27, 2013; Published March 9, 2013
Abstract: Multiple Sclerosis (MS) is an autoimmune disease in which Central Nervous System (CNS) lesions result
from perivascular immune cell infiltration associated with damage to myelin, oligodendrocytes and neurons. CNS
autoimmunity and its regulation are dominated by the inflammatory cytokines IL17 and IFNγ, and the opposing regulatory
cytokines IL10 and the type I IFNs. Toll-like receptors (TLR) play a critical role in modulating cytokine and chemokine
secretion in response to exogenous Pathogen Associated to Molecular Patterns and endogenous Danger-Associated to
Molecular Patterns. Here, we systematically examine the evidence that TLR play a major role in the initiation disease, the
triggering of relapses, and regulation of CNS damage. Data from human studies are supported analyses of a variety of
animal models, including Experimental Autoimmune Encephalomyelitis in TLR-deficient mice. (AJCEI1212003).
Keywords: Multiple sclerosis, toll-like receptors, hygiene hypothesis, microbial flora, gene/environment interactions,
autoimmunity, TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10
Keywords: Multiple sclerosis, toll-like receptors, hygiene hypothesis, microbial flora, gene/environment interactions,
autoimmunity, TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10
Address correspondence to: Dr. Alan G Baxter, Comparative Genomics Centre, Molecular Sciences Building 21, James
Cook University, Townsville, QLD 4811, Australia. Phone: 61-7-4781 6265; Fax: 61-7-4781 6078; E-mail: Alan.Baxter@jcu.
edu.au
Review Article
Role of toll-like receptors in multiple sclerosis
Socorro Miranda-Hernandez, Alan G Baxter
Comparative Genomics Centre, Molecular Sciences Building 21, James Cook University, Townsville, QLD 4811, Australia
Received December 12, 2012; Accepted January 16, 2013; Epub February 27, 2013; Published March 9, 2013
Abstract: Multiple Sclerosis (MS) is an autoimmune disease in which Central Nervous System (CNS) lesions result
from perivascular immune cell infiltration associated with damage to myelin, oligodendrocytes and neurons. CNS
autoimmunity and its regulation are dominated by the inflammatory cytokines IL17 and IFNγ, and the opposing regulatory
cytokines IL10 and the type I IFNs. Toll-like receptors (TLR) play a critical role in modulating cytokine and chemokine
secretion in response to exogenous Pathogen Associated to Molecular Patterns and endogenous Danger-Associated to
Molecular Patterns. Here, we systematically examine the evidence that TLR play a major role in the initiation disease, the
triggering of relapses, and regulation of CNS damage. Data from human studies are supported analyses of a variety of
animal models, including Experimental Autoimmune Encephalomyelitis in TLR-deficient mice. (AJCEI1212003).
Keywords: Multiple sclerosis, toll-like receptors, hygiene hypothesis, microbial flora, gene/environment interactions,
autoimmunity, TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10
Keywords: Multiple sclerosis, toll-like receptors, hygiene hypothesis, microbial flora, gene/environment interactions,
autoimmunity, TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10
Address correspondence to: Dr. Alan G Baxter, Comparative Genomics Centre, Molecular Sciences Building 21, James
Cook University, Townsville, QLD 4811, Australia. Phone: 61-7-4781 6265; Fax: 61-7-4781 6078; E-mail: Alan.Baxter@jcu.
edu.au
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