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Article: TLR7/8 ligand, R-848, inhibits IgE synthesis by acting directly on B lymphocytes

TitleTLR7/8 ligand, R-848, inhibits IgE synthesis by acting directly on B lymphocytes
Authors
Issue Date2008
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJI
Citation
Scandinavian Journal Of Immunology, 2008, v. 67 n. 6, p. 560-568 How to Cite?
AbstractTLRs are involved in the regulation of immune responses. R-848, a TLR7/8 ligand, has potent anti-viral and anti-tumour properties and has been used as a new immune response modifier for enhancing Th1 immune response. In this study, we found that R-848 significantly inhibited IgE synthesis from murine B cells at the single cell levels by anti-CD40 plus IL-4-stimulated splenocytes, in which R-848 acted on the early stage of B cell differentiation to modulate IgE synthesis. This inhibitory effect of R-848 on IgE synthesis was not isotype specific as it also inhibited IgG1 synthesis. Moreover, R-848 had no significant effect on the production of IgG2a by anti-CD40 plus IL-4-stimulated splenocytes. Further studies showed that R-848 markedly promoted murine B cell activation induced by anti-CD40 plus IL-4 by up-regulating the expression of B cell activation markers CD25, CD69 and co-stimulatory molecule CD80. In contrast, R-848 inhibited the proliferation and division of murine B cells in anti-CD40 plus IL-4-stimulated splenocytes. R-848 promoted the production of IFN-γ and IL-12 that were partially responsible for its inhibitory effect on IgE production by anti-CD40 plus IL-4 because the addition of anti-IFN-γ or anti-IL-12 mAbs to the cultures could significantly restore IgE production by splenocytes. Importantly, R-848 had a direct effect on purified B cells to inhibit IgE production induced by anti-CD40 plus IL-4. Taken together, these results demonstrate that R-848 markedly inhibits IgE synthesis, and suggest that R-848 could be used to treat allergic diseases. © 2008 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/129519
ISSN
2015 Impact Factor: 2.27
2015 SCImago Journal Rankings: 0.934
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShen, Een_HK
dc.contributor.authorLu, Len_HK
dc.contributor.authorWu, Cen_HK
dc.date.accessioned2010-12-23T08:38:22Z-
dc.date.available2010-12-23T08:38:22Z-
dc.date.issued2008en_HK
dc.identifier.citationScandinavian Journal Of Immunology, 2008, v. 67 n. 6, p. 560-568en_HK
dc.identifier.issn0300-9475en_HK
dc.identifier.urihttp://hdl.handle.net/10722/129519-
dc.description.abstractTLRs are involved in the regulation of immune responses. R-848, a TLR7/8 ligand, has potent anti-viral and anti-tumour properties and has been used as a new immune response modifier for enhancing Th1 immune response. In this study, we found that R-848 significantly inhibited IgE synthesis from murine B cells at the single cell levels by anti-CD40 plus IL-4-stimulated splenocytes, in which R-848 acted on the early stage of B cell differentiation to modulate IgE synthesis. This inhibitory effect of R-848 on IgE synthesis was not isotype specific as it also inhibited IgG1 synthesis. Moreover, R-848 had no significant effect on the production of IgG2a by anti-CD40 plus IL-4-stimulated splenocytes. Further studies showed that R-848 markedly promoted murine B cell activation induced by anti-CD40 plus IL-4 by up-regulating the expression of B cell activation markers CD25, CD69 and co-stimulatory molecule CD80. In contrast, R-848 inhibited the proliferation and division of murine B cells in anti-CD40 plus IL-4-stimulated splenocytes. R-848 promoted the production of IFN-γ and IL-12 that were partially responsible for its inhibitory effect on IgE production by anti-CD40 plus IL-4 because the addition of anti-IFN-γ or anti-IL-12 mAbs to the cultures could significantly restore IgE production by splenocytes. Importantly, R-848 had a direct effect on purified B cells to inhibit IgE production induced by anti-CD40 plus IL-4. Taken together, these results demonstrate that R-848 markedly inhibits IgE synthesis, and suggest that R-848 could be used to treat allergic diseases. © 2008 The Authors.en_HK
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJIen_HK
dc.relation.ispartofScandinavian Journal of Immunologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntigens, CD40 - antagonists & inhibitors - pharmacologyen_HK
dc.subject.meshB-Lymphocytes - drug effects - immunologyen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshDose-Response Relationship, Immunologicen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHypersensitivity - drug therapyen_HK
dc.subject.meshImidazoles - metabolism - pharmacologyen_HK
dc.subject.meshImmunoglobulin E - biosynthesisen_HK
dc.subject.meshInterferon-gamma - biosynthesisen_HK
dc.subject.meshInterleukin-12 - biosynthesisen_HK
dc.subject.meshInterleukin-4 - pharmacologyen_HK
dc.subject.meshLigandsen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshSpleen - immunologyen_HK
dc.subject.meshToll-Like Receptor 7 - metabolismen_HK
dc.subject.meshToll-Like Receptor 8 - metabolismen_HK
dc.titleTLR7/8 ligand, R-848, inhibits IgE synthesis by acting directly on B lymphocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1365-3083 (Electronic)0300-9475 (Linkin&volume=67&issue=6&spage=560&epage=8&date=2008&atitle=TLR7/8+ligand,+R-848,+inhibits+IgE+synthesis+by+acting+directly+on+B+lymphocytesen_US
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-3083.2008.02105.xen_HK
dc.identifier.pmid18397197-
dc.identifier.scopuseid_2-s2.0-43549113087en_HK
dc.identifier.hkuros176931en_US
dc.identifier.hkuros176932-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-43549113087&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume67en_HK
dc.identifier.issue6en_HK
dc.identifier.spage560en_HK
dc.identifier.epage568en_HK
dc.identifier.eissn1365-3083-
dc.identifier.isiWOS:000255725000004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.citeulike2797894-

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