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Article: B Cell Subsets and Cellular Signatures and Disease Relapse in Lupus Nephritis

TitleB Cell Subsets and Cellular Signatures and Disease Relapse in Lupus Nephritis
Authors
KeywordsB cells
subsets
B cell signatures
lupus nephritis
disease relapse
Issue Date2020
PublisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/immunology
Citation
Frontiers in Immunology, 2020, v. 11, p. article no. 1732 How to Cite?
AbstractIntroduction: Renal relapses adversely affect the long-term outcomes of patients with lupus nephritis (LN), but the pathogenic mechanisms remain elusive. B cell signatures of miR-148a, BACH1, BACH2, and PAX5 expression are relevant to the regulation of B lymphocyte homeostasis. It is unknown whether B cell signature is related to the relapse of LN. Methods: We compared B lymphocyte subsets and cellular signatures during disease quiescence between LN patients with multiple relapses (MR, ≥3 LN relapses within 36 months) and those with no relapse (NR). Also, circulating B lymphocytes were isolated from treatment-naïve patients with active LN and treated with antagomir-148a in vitro to investigate the relationship between miR-148a, BACH1, BACH2, and PAX5. Results: MR patients (n = 19), when compared with NR (n = 14), showed significantly lower percentage of circulating naïve B cells and higher memory B cell-to-naïve B cell ratio. MR patients also showed higher miR-148a levels in sera and B cells, and lower BACH1, BACH2, and PAX5 expression in naïve and memory B cells. Antagomir-148a upregulated BACH1, BACH2, and PAX5 expression, and reduced B cell proliferation upon stimulation, in naïve and memory B cells isolated from treatment-naïve active LN patients. Conclusion: Altered B cell subsets and cellular signatures of miR-148a, BACH1, BACH2, and PAX5 may be associated with distinct patient phenotypes related to the risk of LN relapse.
Persistent Identifierhttp://hdl.handle.net/10722/293394
ISSN
2023 Impact Factor: 5.7
2023 SCImago Journal Rankings: 1.868
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYap, DYH-
dc.contributor.authorYung, SY-
dc.contributor.authorLee, P-
dc.contributor.authorYam, IYL-
dc.contributor.authorTam, C-
dc.contributor.authorTang, C-
dc.contributor.authorChan, TM-
dc.date.accessioned2020-11-23T08:16:07Z-
dc.date.available2020-11-23T08:16:07Z-
dc.date.issued2020-
dc.identifier.citationFrontiers in Immunology, 2020, v. 11, p. article no. 1732-
dc.identifier.issn1664-3224-
dc.identifier.urihttp://hdl.handle.net/10722/293394-
dc.description.abstractIntroduction: Renal relapses adversely affect the long-term outcomes of patients with lupus nephritis (LN), but the pathogenic mechanisms remain elusive. B cell signatures of miR-148a, BACH1, BACH2, and PAX5 expression are relevant to the regulation of B lymphocyte homeostasis. It is unknown whether B cell signature is related to the relapse of LN. Methods: We compared B lymphocyte subsets and cellular signatures during disease quiescence between LN patients with multiple relapses (MR, ≥3 LN relapses within 36 months) and those with no relapse (NR). Also, circulating B lymphocytes were isolated from treatment-naïve patients with active LN and treated with antagomir-148a in vitro to investigate the relationship between miR-148a, BACH1, BACH2, and PAX5. Results: MR patients (n = 19), when compared with NR (n = 14), showed significantly lower percentage of circulating naïve B cells and higher memory B cell-to-naïve B cell ratio. MR patients also showed higher miR-148a levels in sera and B cells, and lower BACH1, BACH2, and PAX5 expression in naïve and memory B cells. Antagomir-148a upregulated BACH1, BACH2, and PAX5 expression, and reduced B cell proliferation upon stimulation, in naïve and memory B cells isolated from treatment-naïve active LN patients. Conclusion: Altered B cell subsets and cellular signatures of miR-148a, BACH1, BACH2, and PAX5 may be associated with distinct patient phenotypes related to the risk of LN relapse.-
dc.languageeng-
dc.publisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/immunology-
dc.relation.ispartofFrontiers in Immunology-
dc.rightsThis Document is Protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectB cells-
dc.subjectsubsets-
dc.subjectB cell signatures-
dc.subjectlupus nephritis-
dc.subjectdisease relapse-
dc.titleB Cell Subsets and Cellular Signatures and Disease Relapse in Lupus Nephritis-
dc.typeArticle-
dc.identifier.emailYap, DYH: desmondy@hku.hk-
dc.identifier.emailYung, SY: ssyyung@hku.hk-
dc.identifier.emailLee, P: pl85@hku.hk-
dc.identifier.emailYam, IYL: iylyam@hkucc.hku.hk-
dc.identifier.emailTam, C: ct0060@hku.hk-
dc.identifier.emailTang, C: csotang@hkucc.hku.hk-
dc.identifier.emailChan, TM: dtmchan@hkucc.hku.hk-
dc.identifier.authorityYap, DYH=rp01607-
dc.identifier.authorityYung, SY=rp00455-
dc.identifier.authorityChan, TM=rp00394-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3389/fimmu.2020.01732-
dc.identifier.pmid33013825-
dc.identifier.pmcidPMC7511550-
dc.identifier.scopuseid_2-s2.0-85091482505-
dc.identifier.hkuros320065-
dc.identifier.volume11-
dc.identifier.spagearticle no. 1732-
dc.identifier.epagearticle no. 1732-
dc.identifier.isiWOS:000574612800001-
dc.publisher.placeSwitzerland-
dc.identifier.issnl1664-3224-

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