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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005392naa a2200505 4500
001oai:DiVA.org:uu-313542
003SwePub
008170120s2016 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:134810300
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3135422 URI
0247 a https://doi.org/10.1186/s13075-016-1181-02 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1348103002 URI
040 a (SwePub)uud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Joshua, Vijayu Karolinska Institutet4 aut
2451 0a Antibody responses to de novo identified citrullinated fibrinogen peptides in rheumatoid arthritis and visualization of the corresponding B cells
264 c 2016-12-01
264 1b Springer Science and Business Media LLC,c 2016
338 a electronic2 rdacarrier
520 a Background: Antibodies against citrullinated proteins (ACPA) are common in patients with rheumatoid arthritis (RA). ACPA can appear before disease onset and target many self-antigens. Citrullinated fibrin/fibrinogen represents a classical ACPA target antigen, and mass spectrometry of RA synovial fluid reveals elevated citrullinated (cit) fibrinogen (Fib) peptides compared to non-RA controls. We investigated the extent to which these less-studied peptides represent autoantibody targets and sought to visualize the corresponding cit-Fib-reactive B cells in RA patients. Methods: An in-house ELISA was established against four cit-Fib alpha-subunit peptides (cit-Fib alpha-35; cit-Fib alpha-216,218; cit-Fib alpha-263,271 and cit-Fib alpha-425,426) and serum from patients with established RA (n = 347) and disease controls with psoriatic arthritis (PsA) or ankylosing spondylitis (AS) (n = 236) were analyzed. RA patients were genotyped for HLA-DR alleles, PTPN22 R620W and screened for anti-CCP2 and cit-Fib protein antibodies. The cit-Fib peptides were also used to assemble antigen tetramers to identify cit-Fib-reactive B cells in peripheral blood by flow cytometry. Results: The frequencies of autoantibodies against different cit-Fib epitopes in RA patients compared to PsA/AS patients were: cit-Fib alpha-35 (RA 20%, vs PsA/AS 1%); cit-Fib alpha-216,218 (13% vs 0.5%); cit-Fib alpha-263,271 (21% vs 0.5%) and cit-Fib alpha-425,426 (17% vs 1%). The presence of autoantibodies against these peptides was associated with presence of anti-CCP2 and anti-cit-Fib protein antibodies. No association was found between HLA-DR shared epitope and antibodies to the different cit-Fib peptides. However, association was observed between the PTPN22 risk allele and positivity to cit-Fib alpha-35 and cit-Fib alpha-263,271. B cells carrying surface Ig reactive to these cit-Fib peptides were found in RA peripheral blood and these tend to be more common in PTPN22 risk allele carriers. Conclusions: Our data show that several cit-Fib peptides are targeted by autoantibodies in RA, but not in PsA/AS, implicating that these are not due to arthritis but more specific for RA etiology. The RA-associated anti-cit protein response is broad with many parallel immune responses. The association between cit-Fib autoantibodies and the PTPN22 R620W risk allele supports the hypothesis of altered B cell regulation, such as autoreactive B cells evading tolerance checkpoints.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng
653 a Rheumatoid arthritis
653 a Autoantibodies
653 a Fibrinogen
653 a ACPA
653 a PTPN22
7001 a Schobers, Loesu Radboud Univ Nijmegen, Dept Biomol Chem, Radboud Inst Mol Life Sci, Nijmegen, Netherlands.;Radboud Univ Nijmegen, Inst Mol & Mat, Nijmegen, Netherlands.4 aut
7001 a Titcombe, Philip J.u Karolinska Univ Hosp Solna, Karolinska Inst, Dept Med, Rheumatol Unit, S-17176 Stockholm, Sweden.4 aut
7001 a Israelsson, Lenau Karolinska Institutet4 aut
7001 a Rönnelid, Johanu Uppsala universitet,Klinisk immunologi4 aut0 (Swepub:uu)joharonn
7001 a Hansson, Monikau Karolinska Institutet4 aut
7001 a Catrina, Anca I.u Karolinska Institutet4 aut
7001 a Pruijn, Ger J. M.u Radboud Univ Nijmegen, Dept Biomol Chem, Radboud Inst Mol Life Sci, Nijmegen, Netherlands.;Radboud Univ Nijmegen, Inst Mol & Mat, Nijmegen, Netherlands.4 aut
7001 a Malmstrom, Vivianneu Karolinska Institutet4 aut
7102 a Karolinska Institutetb Radboud Univ Nijmegen, Dept Biomol Chem, Radboud Inst Mol Life Sci, Nijmegen, Netherlands.;Radboud Univ Nijmegen, Inst Mol & Mat, Nijmegen, Netherlands.4 org
7730 t ARTHRITIS RESEARCH & THERAPYd : Springer Science and Business Media LLCg 18q 18x 1478-6354x 1478-6362
8564 u https://uu.diva-portal.org/smash/get/diva2:1070101/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u https://arthritis-research.biomedcentral.com/track/pdf/10.1186/s13075-016-1181-0
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-313542
8564 8u https://doi.org/10.1186/s13075-016-1181-0
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:134810300

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