Abstract
Pattern recognition receptors (PRRs) coordinate the innate immune response and have a significant role in the development of multiple sclerosis (MS). Accumulating evidence has identified both pathogenic and protective functions of PRR signaling in MS and its animal model, experimental autoimmune encephalomyelitis (EAE). Additionally, evidence for PRR signaling in non-immune cells and PRR responses to host-derived endogenous ligands has also revealed new pathways controlling the development of CNS autoimmunity. Many PRRs remain uncharacterized in MS and EAE, and understanding the distinct triggers and functions of PRR signaling in CNS autoimmunity requires further investigation. In this brief review, we discuss the diverse pathogenic and protective functions of PRRs in MS and EAE, and highlight major avenues for future research.
Highlights
Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system (CNS) characterized by neuroinflammation, demyelination, and axon damage
Despite similar EAE severity between Tlr2−/− and wild-type mice in some reports [19, 20], and other results suggesting the pathogenicity of TLR2 [18, 21, 22], more recent studies indicate TLR2 stimulation may be protective
NLRX1 suppresses NFκB induced by Toll-like receptors (TLRs) signaling [65, 66] and Nlrx1−/− mice are more susceptible to EAE [67] due to hyperactivation of myeloid cells in the CNS [67]
Summary
Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system (CNS) characterized by neuroinflammation, demyelination, and axon damage. Despite similar EAE severity between Tlr2−/− and wild-type mice in some reports [19, 20], and other results suggesting the pathogenicity of TLR2 [18, 21, 22], more recent studies indicate TLR2 stimulation may be protective. Tlr2−/− mice developed reduced pathology in the cuprizone demyelination model, suggesting a pathogenic role for basal TLR2 signaling in the absence of exogenous stimulation [15, 23].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
