Role of the galactosyl moiety of collagen glycopeptides for T-cell stimulation in a model for rheumatoid arthritis
(2003) In Bioorganic & Medicinal Chemistry 11(18). p.3981-3987- Abstract
- Two protected derivatives of beta-D-galactopyranosyl-5-hydroxy-L-lysine, in which HO-4 of galactose has been O-methylated or replaced by fluorine, have been prepared. The building blocks were incorporated at position 264 of the peptide fragment CII259-273 from type II collagen by solid-phase synthesis. The ability of these two glycopeptides, and two CII259-273 glycopeptides in which HO-4 of galactose was either unmodified or deoxygenated, to elicit responses from T-cell hybridomas obtained in a mouse model for rheumatoid arthritis was then determined. The hybridomas were all highly sensitive towards modifications at C-4 of the beta-D-galactosyl residue of CII259-273, highlighting the role of HO-4 as an important contact point for the... (More)
- Two protected derivatives of beta-D-galactopyranosyl-5-hydroxy-L-lysine, in which HO-4 of galactose has been O-methylated or replaced by fluorine, have been prepared. The building blocks were incorporated at position 264 of the peptide fragment CII259-273 from type II collagen by solid-phase synthesis. The ability of these two glycopeptides, and two CII259-273 glycopeptides in which HO-4 of galactose was either unmodified or deoxygenated, to elicit responses from T-cell hybridomas obtained in a mouse model for rheumatoid arthritis was then determined. The hybridomas were all highly sensitive towards modifications at C-4 of the beta-D-galactosyl residue of CII259-273, highlighting the role of HO-4 as an important contact point for the T-cell receptor. Most likely, this glycopeptide hydroxyl group is involved in hydrogen bonding with the T-cell receptor. (C) 2003 Elsevier Ltd. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/302328
- author
- Holm, B ; Baquer, SM ; Holm, L ; Holmdahl, Rikard LU and Kihlberg, J
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Bioorganic & Medicinal Chemistry
- volume
- 11
- issue
- 18
- pages
- 3981 - 3987
- publisher
- Elsevier
- external identifiers
-
- wos:000185037900015
- pmid:12927859
- scopus:0043092066
- ISSN
- 0968-0896
- DOI
- 10.1016/S0968-0896(03)00407-3
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)
- id
- b7ef5824-7336-4096-8cd1-3a712c4eabcb (old id 302328)
- date added to LUP
- 2016-04-01 12:30:48
- date last changed
- 2022-02-03 23:12:47
@article{b7ef5824-7336-4096-8cd1-3a712c4eabcb, abstract = {{Two protected derivatives of beta-D-galactopyranosyl-5-hydroxy-L-lysine, in which HO-4 of galactose has been O-methylated or replaced by fluorine, have been prepared. The building blocks were incorporated at position 264 of the peptide fragment CII259-273 from type II collagen by solid-phase synthesis. The ability of these two glycopeptides, and two CII259-273 glycopeptides in which HO-4 of galactose was either unmodified or deoxygenated, to elicit responses from T-cell hybridomas obtained in a mouse model for rheumatoid arthritis was then determined. The hybridomas were all highly sensitive towards modifications at C-4 of the beta-D-galactosyl residue of CII259-273, highlighting the role of HO-4 as an important contact point for the T-cell receptor. Most likely, this glycopeptide hydroxyl group is involved in hydrogen bonding with the T-cell receptor. (C) 2003 Elsevier Ltd. All rights reserved.}}, author = {{Holm, B and Baquer, SM and Holm, L and Holmdahl, Rikard and Kihlberg, J}}, issn = {{0968-0896}}, language = {{eng}}, number = {{18}}, pages = {{3981--3987}}, publisher = {{Elsevier}}, series = {{Bioorganic & Medicinal Chemistry}}, title = {{Role of the galactosyl moiety of collagen glycopeptides for T-cell stimulation in a model for rheumatoid arthritis}}, url = {{http://dx.doi.org/10.1016/S0968-0896(03)00407-3}}, doi = {{10.1016/S0968-0896(03)00407-3}}, volume = {{11}}, year = {{2003}}, }