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Liver X receptor activation decreases the severity of experimental autoimmune encephalomyelitis
Author(s) -
Hindinger Claudia,
Hinton David R.,
Kirwin Stefanie J.,
Atkinson Roscoe D.,
Burnett Margaret E.,
Bergmann Cornelia C.,
Stohlman Stephen A.
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21038
Subject(s) - experimental autoimmune encephalomyelitis , proinflammatory cytokine , liver x receptor , agonist , microglia , inflammation , encephalomyelitis , receptor , cytokine , immunology , t cell , biology , major histocompatibility complex , central nervous system , endocrinology , nuclear receptor , medicine , immune system , biochemistry , gene , transcription factor
Abstract Agonists of liver X receptors (LXR), members of the nuclear hormone receptor superfamily, alter secretion of proinflammatory cytokines, suggesting potential antiinflammatory effects. A synthetic LXR agonist inhibited T‐cell proliferation and cytokine release in a dose‐dependent manner. Treatment of mice during induction of experimental autoimmune encephalomyelitis reduced clinical symptoms, central nervous system cellular inflammation, and major histocompatibility class II expression on microglia, as well as demyelination. In contrast to in vitro analysis, no reductions in peripheral neuroantigen specific T‐cell responses were detected in comparing ligand and vehicle treated mice. These data suggest that LXR agonists play an important protective role in the regulation of T‐cell‐mediated inflammatory disease of the central nervous system. © 2006 Wiley‐Liss, Inc.