Integration of lectin-glycan recognition systems and immune cell networks in CNS inflammation

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• 作者：Santiago P. Mendez-Huergo^aAuthor Vitae ; Sebastiá ; n M. Maller^aAuthor Vitae ; Mauricio F. Farez^bAuthor Vitae ; Karina Mariñ ; o^cAuthor Vitae ; Jorge Correale^bAuthor Vitae ; Gabriel A. Rabinovich^a ; ^d ; ^{gabriel.r@ibyme.conicet.gov.ar" class="auth_mail} ; ^{gabyrabi@gmail.com" class="auth_mail}Author Vitae
• 关键词：BBB ; blood&ndash ; brain barrier ; CLR ; C-type lectin receptors ; CNS ; central nervous system ; CRD ; carbohydrate recognition domain ; CTLA-4 ; cytotoxic T lymphocyte antigen-4 ; DCs ; dendritic cells ; EAE ; experimental autoimmune encephalomyelitis ; MGAT5 ; 尾1 ; 6 N-acetylglucosaminyltransferase 5 ; MOG ; myelin oligodendrocyte glycoprotein ; MS ; multiple sclerosis ; PP-MS ; primary progressive multiple sclerosis ; RR-MS ; relapsing remitting multiple sclerosis ; S1P ; sphingosine 1-phosphate ; Sn ; sialoadhesin ; SP-M
• 刊名：Cytokine and Growth Factor Reviews
• 出版年：June 2014
• 年：2014
• 卷：25
• 期：3
• 页码：247-255
• 全文大小：1162 K

文摘

Multiple sclerosis (MS) is a progressive degenerative disorder of the central nervous system (CNS), characterized by inflammation, demyelination and axonal loss. While the majority of MS patients experience relapsing-remitting symptoms followed by a secondary progressive phase, about 10–15% patients exhibit a primary progressive disease involving continuous progression from its onset. Here we review the role of lectin–glycan recognition systems, including those concerning siglecs, C-type lectins and galectins in the pathogenesis of MS and experimental autoimmune encephalomyelitis. Particularly, we will focus on the role of galectins in the fate of T cells, dendritic cells and CNS cell populations. Understanding the regulatory circuits governed by lectin–glycan interactions and their association with disease-associated cytokine networks will contribute to develop novel therapeutic strategies in MS.