InChI=1S/C48H91NO11S/c1- 3-5-7-9-11-13-15-17-18-19-20-21-22-23-24-26-28-30-32-34-36-38-44(52)49-41(42(51)37-35-33-31-29-27-25-16-14-12-10-8-6-4-2)40-58-48-46(54)47(60-61(55,56)57)45(53)43(39-50)59-48/h17-18,35,37,41-43,45-48,50-51,53-54H,3-16,19-34,36,38-40H2,1-2H3,(H,49,52)(H,55,56,57)/b18-17-,37-35+/t41-,42+,43+,45-,46+,47-,48+/m0/s1 |
| ZZQWQNAZXFNSEP-JCOQVFCVSA-N |
| CCCCCCCCCCCCC\C=C\[C@@H](O)[C@H](CO[C@@H]1O[C@H](CO)[C@H](O)[C@H](OS(O)(=O)=O)[C@H]1O)NC(=O)CCCCCCCCCCCCC\C=C/CCCCCCCC |
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epitope
The biological role played by a material entity when bound by a receptor of the adaptive immune system. Specific site on an antigen to which an antibody binds.
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
(via galactosylceramide sulfate )
human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
(via N-acyl-beta-D-galactosylsphingosine )
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View more via ChEBI Ontology
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Outgoing
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1-(3-O-sulfo-β-D-galactosyl)-N-[(15Z)-tetracos-15-enoyl]sphingosine
(CHEBI:41539)
has role
epitope
(CHEBI:53000)
1-(3-O-sulfo-β-D-galactosyl)-N-[(15Z)-tetracos-15-enoyl]sphingosine
(CHEBI:41539)
is a
N-acyl-β-D-galactosylsphingosine
(CHEBI:18390)
1-(3-O-sulfo-β-D-galactosyl)-N-[(15Z)-tetracos-15-enoyl]sphingosine
(CHEBI:41539)
is a
galactosylceramide sulfate
(CHEBI:18318)
1-(3-O-sulfo-β-D-galactosyl)-N-[(15Z)-tetracos-15-enoyl]sphingosine
(CHEBI:41539)
is conjugate acid of
1-(3-O-sulfo-β-D-galactosyl)-N-[(15Z)-tetracos-15-enoyl]sphingosine(1−)
(CHEBI:139139)
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Incoming
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1-(3-O-sulfo-β-D-galactosyl)-N-[(15Z)-tetracos-15-enoyl]sphingosine(1−)
(CHEBI:139139)
is conjugate base of
1-(3-O-sulfo-β-D-galactosyl)-N-[(15Z)-tetracos-15-enoyl]sphingosine
(CHEBI:41539)
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(15Z)-N-{(2S,3R,4E)-3-hydroxy-1-[(3-O-sulfo-β-D-galactopyranosyl)oxy]octadec-4-en-2-yl}tetracos-15-enamide
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(15Z)-N-((1S,2R,3E)-2-HYDROXY-1-{[(3-O-SULFO-BETA-D-GALACTOPYRANOSYL)OXY]METHYL}HEPTADEC-3-ENYL)TETRACOS-15-ENAMIDE
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PDBeChem
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(2S,3R,4E)-N-NERVONIC-1-[BETA-D-(3-SULFATE)-GALACTOPYRANOSYL]-2-AMINO-OCTADECENE-3-OL CIS-TETRACOSENOYL SULFATIDE
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PDBeChem
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(3'-sulfo)Galβ-Cer(d18:1/24:1(15Z))
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LIPID MAPS
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3-O-sulfo-D-galactosyl-β1-1'-N-nervonoyl-D-erythro-sphingosine
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ChEBI
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3-O-Sulfogalactosylceramide (d18:1/24:1(15Z))
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HMDB
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C24:1 mono-sulfo galactosyl(β) ceramide (d18:1/24:1)
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ChEBI
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C24:1 Sulfatide
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LIPID MAPS
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sulfatide C24:1
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ChEBI
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Birkinshaw RW, Pellicci DG, Cheng TY, Keller AN, Sandoval-Romero M, Gras S, de Jong A, Uldrich AP, Moody DB, Godfrey DI, Rossjohn J (2015)
αβ T cell antigen receptor recognition of CD1a presenting self lipid ligands.
Nature immunology 16, 258-266 [PubMed:25642819]
[show Abstract]
A central paradigm in αβ T cell-mediated immunity is the simultaneous co-recognition of antigens and antigen-presenting molecules by the αβ T cell antigen receptor (TCR). CD1a presents a broad repertoire of lipid-based antigens. We found that a prototypical autoreactive TCR bound CD1a when it was presenting a series of permissive endogenous ligands, while other lipid ligands were nonpermissive to TCR binding. The structures of two TCR-CD1a-lipid complexes showed that the TCR docked over the A' roof of CD1a in a manner that precluded direct contact with permissive ligands. Nonpermissive ligands indirectly inhibited TCR binding by disrupting the TCR-CD1a contact zone. The exclusive recognition of CD1a by the TCR represents a previously unknown mechanism whereby αβ T cells indirectly sense self antigens that are bound to an antigen-presenting molecule. | Girardi E, Maricic I, Wang J, Mac TT, Iyer P, Kumar V, Zajonc DM (2012)
Type II natural killer T cells use features of both innate-like and conventional T cells to recognize sulfatide self antigens.
Nature immunology 13, 851-856 [PubMed:22820602]
[show Abstract]
Glycolipids presented by the major histocompatibility complex (MHC) class I homolog CD1d are recognized by natural killer T cells (NKT cells) characterized by either a semi-invariant T cell antigen receptor (TCR) repertoire (type I NKT cells or iNKT cells) or a relatively variable TCR repertoire (type II NKT cells). Here we describe the structure of a type II NKT cell TCR in complex with CD1d-lysosulfatide. Both TCR α-chains and TCR β-chains made contact with the CD1d molecule with a diagonal footprint, typical of MHC-TCR interactions, whereas the antigen was recognized exclusively with a single TCR chain, similar to the iNKT cell TCR. Type II NKT cell TCRs, therefore, recognize CD1d-sulfatide complexes by a distinct recognition mechanism characterized by the TCR-binding features of both iNKT cells and conventional peptide-reactive T cells. | Girardi E, Wang J, Mac TT, Versluis C, Bhowruth V, Besra G, Heck AJ, Van Rhijn I, Zajonc DM (2010)
Crystal structure of bovine CD1b3 with endogenously bound ligands.
Journal of immunology (Baltimore, Md. : 1950) 185, 376-386 [PubMed:20519644]
[show Abstract]
The CD1 family of Ag-presenting molecules is able to display lipids to T cells by binding them within a hydrophobic groove connected to the protein surface. In particular, the CD1b isotype is capable of binding ligands with greatly varying alkyl chain lengths through a complex network of interconnected hydrophobic pockets. Interestingly, mycobacterial lipids such as glucose monomycolate exclusively bind to CD1b. We determined the crystal structure of one of the three expressed bovine CD1b proteins, CD1b3, in complex with endogenous ligands, identified by mass spectrometry as a mixture of phosphatidylcholine and phosphatidylethanolamine, and analyzed the ability of the protein to bind glycolipids in vitro. The structure reveals a complex binding groove architecture, similar to the human ortholog but with consequential differences. Intriguingly, in bovine CD1b3 only the A', C' and F' pockets are present, whereas the T' pocket previously described in human CD1b is closed. This different pocket conformation could affect the ability of boCD1b3 to recognize lipids with long acyl chains such as glucose monomycolate. However, even in the absence of a T' tunnel, bovine CD1b3 is able to bind mycolates from Rhodococcus ruber in vitro. | Zajonc DM, Maricic I, Wu D, Halder R, Roy K, Wong CH, Kumar V, Wilson IA (2005)
Structural basis for CD1d presentation of a sulfatide derived from myelin and its implications for autoimmunity.
The Journal of experimental medicine 202, 1517-1526 [PubMed:16314439]
[show Abstract]
Sulfatide derived from the myelin stimulates a distinct population of CD1d-restricted natural killer T (NKT) cells. Cis-tetracosenoyl sulfatide is one of the immunodominant species in myelin as identified by proliferation, cytokine secretion, and CD1d tetramer staining. The crystal structure of mouse CD1d in complex with cis-tetracosenoyl sulfatide at 1.9 A resolution reveals that the longer cis-tetracosenoyl fatty acid chain fully occupies the A' pocket of the CD1d binding groove, whereas the sphingosine chain fills up the F' pocket. A precise hydrogen bond network in the center of the binding groove orients and positions the ceramide backbone for insertion of the lipid tails in their respective pockets. The 3'-sulfated galactose headgroup is highly exposed for presentation to the T cell receptor and projects up and away from the binding pocket due to its beta linkage, compared with the more intimate binding of the alpha-glactosyl ceramide headgroup to CD1d. These structure and binding data on sulfatide presentation by CD1d have important implications for the design of therapeutics that target T cells reactive for myelin glycolipids in autoimmune diseases of the central nervous system. |
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