File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Roles of B Cell-Intrinsic TLR Signals in Systemic Lupus Erythematosus

TitleRoles of B Cell-Intrinsic TLR Signals in Systemic Lupus Erythematosus
Authors
KeywordsAnti-nuclear autoantibody (ANA)
B-1 B cells
Germinal center B cells (GC B cells)
Marginal zone B cells (MZ B cells)
Memory B cells
Myeloid differentiation primary response gene 88 (MyD88)
Systemic lupus erythematosus (SLE)
Toll-like receptor (TLR)
Transitional B cells
Unc-93 Homolog B1 (C. elegans) (Unc93b1)
Issue Date2015
PublisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms
Citation
International Journal of Molecular Sciences, 2015, v. 16 n. 6, p. 13084-13105 How to Cite?
AbstractToll-like receptors (TLRs) are a large family of pattern recognition receptors. TLR signals are involved in the pathogenesis of systemic lupus erythematosus. Mouse and human B cells constitutively express most TLRs. Many B cell subpopulations are highly responsive to certain TLR ligation, including B-1 B cells, transitional B cells, marginal zone B cells, germinal center B cell and memory B cells. The B cell-intrinsic TLR signals play critical roles during lupus process. In this review, roles of B cell-intrinsic TLR2, 4, 7, 8 and 9 signals are discussed during lupus pathogenesis in both mouse model and patients. Moreover, mechanisms underlying TLR ligation-triggered B cell activation and signaling pathways are highlighted.
Persistent Identifierhttp://hdl.handle.net/10722/212118
ISSN
2021 Impact Factor: 6.208
2020 SCImago Journal Rankings: 1.455
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMa, K-
dc.contributor.authorLi, J-
dc.contributor.authorFang, Y-
dc.contributor.authorLu, L-
dc.date.accessioned2015-07-21T02:23:35Z-
dc.date.available2015-07-21T02:23:35Z-
dc.date.issued2015-
dc.identifier.citationInternational Journal of Molecular Sciences, 2015, v. 16 n. 6, p. 13084-13105-
dc.identifier.issn1422-0067-
dc.identifier.urihttp://hdl.handle.net/10722/212118-
dc.description.abstractToll-like receptors (TLRs) are a large family of pattern recognition receptors. TLR signals are involved in the pathogenesis of systemic lupus erythematosus. Mouse and human B cells constitutively express most TLRs. Many B cell subpopulations are highly responsive to certain TLR ligation, including B-1 B cells, transitional B cells, marginal zone B cells, germinal center B cell and memory B cells. The B cell-intrinsic TLR signals play critical roles during lupus process. In this review, roles of B cell-intrinsic TLR2, 4, 7, 8 and 9 signals are discussed during lupus pathogenesis in both mouse model and patients. Moreover, mechanisms underlying TLR ligation-triggered B cell activation and signaling pathways are highlighted.-
dc.languageeng-
dc.publisherMolecular Diversity Preservation International. The Journal's web site is located at http://www.mdpi.org/ijms-
dc.relation.ispartofInternational Journal of Molecular Sciences-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAnti-nuclear autoantibody (ANA)-
dc.subjectB-1 B cells-
dc.subjectGerminal center B cells (GC B cells)-
dc.subjectMarginal zone B cells (MZ B cells)-
dc.subjectMemory B cells-
dc.subjectMyeloid differentiation primary response gene 88 (MyD88)-
dc.subjectSystemic lupus erythematosus (SLE)-
dc.subjectToll-like receptor (TLR)-
dc.subjectTransitional B cells-
dc.subjectUnc-93 Homolog B1 (C. elegans) (Unc93b1)-
dc.titleRoles of B Cell-Intrinsic TLR Signals in Systemic Lupus Erythematosus-
dc.typeArticle-
dc.identifier.emailMa, K: kongyang@hku.hk-
dc.identifier.emailLu, L: liweilu@hkucc.hku.hk-
dc.identifier.authorityLu, L=rp00477-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3390/ijms160613084-
dc.identifier.pmid26068236-
dc.identifier.pmcidPMC4490487-
dc.identifier.scopuseid_2-s2.0-84931269995-
dc.identifier.hkuros245001-
dc.identifier.volume16-
dc.identifier.issue6-
dc.identifier.spage13084-
dc.identifier.epage13105-
dc.identifier.isiWOS:000357492800071-
dc.publisher.placeSwitzerland-
dc.identifier.issnl1422-0067-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats