Taxonomic group: fungi / Basidiomycota
(Phylum: Basidiomycota)
Organ / tissue: capsuleAssociated disease: infection due to Cryptococcus neoformans [ICD11:
XN3EH 
]
The structure was elucidated in this paperNCBI PubMed ID: 30131805Publication DOI: 10.3389/fimmu.2018.01781Journal NLM ID: 101560960Publisher: Lausanne: Frontiers Research Foundation
Correspondence: Jia XM <jiaxm
tongji.edu.cn>; Xu JF <jfxucn
gmail.com>
Institutions: Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China, Department of Respiratory and Critical Care Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China
Cryptococcus neoformans and Cryptococcus gattii cause life-threatening meningoencephalitis or lung diseases in immunocompetent individuals or immunocompromised ones. C. neoformans and C. gattii are subdivided into five serotypes based on their capsular glucuronoxylomannan (GXM). C. neoformans consists of serotypes A, D, and AD hybrid, and C. gattii consists of serotypes B and C. Given structural differences of GXM between C. neoformans and C. gattii, it remains unclear that how innate immune system recognizes GXM. Here, we report that C-type lectin receptor Dectin-3 (MCL encoded by Clec4d) is a direct receptor for GXMs from C. neoformans serotype AD (C.n-AD) and C. gattii serotype B (C.g-B). GXMs from C.n-AD and C.g-B activated NF-κB and ERK pathways to induce pro-inflammatory cytokine production, whereas it was completely abolished due to deficiency of Dectin-3 or caspase recruitment domain family member 9 (CARD9). Upon pulmonary C.n-AD and C.g-B infection, Dectin-3- and CARD9-deficient mice were highly susceptible and showed augmented lung injury due to impairment of alveolar macrophage accumulation and killing activities. Our study provides the first biological and genetic evidence demonstrating that Dectin-3 recognizes GXM of C.n-AD and C.g-B to initiate host defense against cryptococcosis.
innate immunity, Glucuronoxylomannan, C-type lectin receptor, Crytococcus, Dectin-3
Structure type: suggested polymer biological repeating unit
Location inside paper: Fig. 3 (GXM-A), Fig. S2(E)
Trivial name: glucuronoxylomannan (GXM)
Compound class: CPS, EPS, O-polysaccharide, O-antigen, cell wall polysaccharide, polysaccharide, glucuronoxylomannan, capsule polysaccharide
Contained glycoepitopes: IEDB_114701,IEDB_115136,IEDB_115576,IEDB_130701,IEDB_140116,IEDB_140630,IEDB_144983,IEDB_145668,IEDB_152206,IEDB_164174,IEDB_167188,IEDB_174332,IEDB_2270799,IEDB_423153,IEDB_76933,IEDB_983930,SB_197,SB_44,SB_67,SB_72
Methods: 1H NMR, GC-MS, ELISA, biological assays, immunoblotting, acetylation, NaBH4 reduction, dialysis, flow cytometry, phenol-sulfuric acid assay, centrifugation, TFA hydrolysis
Biological activity: activates TLR-4-mediated intracellular signaling
Related record ID(s): 48719, 48721, 48722, 48723, 48724
NCBI Taxonomy refs (TaxIDs): 235443Reference(s) to other database(s): GTC:G75580HK, CCSD:
50376, CBank-STR:15059
Show glycosyltransferases
NMR conditions: in D2O at 298(H) K
[as TSV]
1H NMR data: present in publication
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There is only one chemically distinct structure:
Found 
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