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Accession Number ADA575594
Title Targeting Chemerin Receptor CMKLR1 in Multiple Sclerosis.
Publication Date Sep 2012
Media Count 69p
Personal Author B. Zabel
Abstract Therapies that target leukocyte trafficking pathways can reduce disease activity and improve clinical outcomes in multiple sclerosis (MS). Experimental autoimmune encephalomyelitis (EAE) is a widely studied animal model that shares many clinical and histological features with human MS. Chemokine-like receptor-1 (CMKLR1) is a chemoattractant receptor that is expressed by key effector cells in EAE and MS, including macrophages, subsets of dendritic cells, natural killer cells and microglia. CMKLR1-deficient mice develop less severe clinical and histological EAE than wild-type mice. In this study, we identified alphanaphthoyl ethyltrimethylammonium iodide (alpha-NETA) as a selective CMKLR1 small molecule antagonist that inhibits chemerin- triggered CMKLR1+ cell migration. Prophylactic dosing with alpha-NETA significantly delayed the onset of EAE induced in C57BL/6 mice. In addition, alpha-NETA treatment significantly inhibited accumulation of inflammatory leukocytes within the CNS. This study provides additional proof-of-concept data that targeting CMKLR1:chemerin interactions may be beneficial in preventing or treating MS.
Keywords Autoimmunization
Central nervous system
Clinical medicine
Cmklr1(Chemokine-like receptor-1)
Experimental autoimmune encephalomyelitis
Ms(Multiple sclerosis)
Preventive medicine
Receptor sites(Physiology)
Sense organs

Source Agency Non Paid ADAS
NTIS Subject Category 57A - Anatomy
57S - Physiology
57E - Clinical Medicine
Corporate Author Palo Alto Inst. for Research and Education, Inc., CA.
Document Type Technical report
Title Note Annual rept. 29 Aug 2011-28 Aug 2012.
NTIS Issue Number 1319
Contract Number W81XWH-11-1-0512

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