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- Publisher Website: 10.1111/j.1365-3083.2008.02105.x
- Scopus: eid_2-s2.0-43549113087
- PMID: 18397197
- WOS: WOS:000255725000004
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Article: TLR7/8 ligand, R-848, inhibits IgE synthesis by acting directly on B lymphocytes
Title | TLR7/8 ligand, R-848, inhibits IgE synthesis by acting directly on B lymphocytes |
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Authors | |
Issue Date | 2008 |
Publisher | Blackwell 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? |
Abstract | TLRs 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 Identifier | http://hdl.handle.net/10722/129519 |
ISSN | 2023 Impact Factor: 4.1 2023 SCImago Journal Rankings: 0.946 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Shen, E | en_HK |
dc.contributor.author | Lu, L | en_HK |
dc.contributor.author | Wu, C | en_HK |
dc.date.accessioned | 2010-12-23T08:38:22Z | - |
dc.date.available | 2010-12-23T08:38:22Z | - |
dc.date.issued | 2008 | en_HK |
dc.identifier.citation | Scandinavian Journal Of Immunology, 2008, v. 67 n. 6, p. 560-568 | en_HK |
dc.identifier.issn | 0300-9475 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/129519 | - |
dc.description.abstract | TLRs 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.language | eng | en_US |
dc.publisher | Blackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/SJI | en_HK |
dc.relation.ispartof | Scandinavian Journal of Immunology | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Antigens, CD40 - antagonists & inhibitors - pharmacology | en_HK |
dc.subject.mesh | B-Lymphocytes - drug effects - immunology | en_HK |
dc.subject.mesh | Cells, Cultured | en_HK |
dc.subject.mesh | Dose-Response Relationship, Immunologic | en_HK |
dc.subject.mesh | Female | en_HK |
dc.subject.mesh | Hypersensitivity - drug therapy | en_HK |
dc.subject.mesh | Imidazoles - metabolism - pharmacology | en_HK |
dc.subject.mesh | Immunoglobulin E - biosynthesis | en_HK |
dc.subject.mesh | Interferon-gamma - biosynthesis | en_HK |
dc.subject.mesh | Interleukin-12 - biosynthesis | en_HK |
dc.subject.mesh | Interleukin-4 - pharmacology | en_HK |
dc.subject.mesh | Ligands | en_HK |
dc.subject.mesh | Mice | en_HK |
dc.subject.mesh | Mice, Inbred BALB C | en_HK |
dc.subject.mesh | Spleen - immunology | en_HK |
dc.subject.mesh | Toll-Like Receptor 7 - metabolism | en_HK |
dc.subject.mesh | Toll-Like Receptor 8 - metabolism | en_HK |
dc.title | TLR7/8 ligand, R-848, inhibits IgE synthesis by acting directly on B lymphocytes | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+lymphocytes | en_US |
dc.identifier.email | Lu, L:liweilu@hkucc.hku.hk | en_HK |
dc.identifier.authority | Lu, L=rp00477 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1111/j.1365-3083.2008.02105.x | en_HK |
dc.identifier.pmid | 18397197 | - |
dc.identifier.scopus | eid_2-s2.0-43549113087 | en_HK |
dc.identifier.hkuros | 176931 | en_US |
dc.identifier.hkuros | 176932 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-43549113087&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 67 | en_HK |
dc.identifier.issue | 6 | en_HK |
dc.identifier.spage | 560 | en_HK |
dc.identifier.epage | 568 | en_HK |
dc.identifier.eissn | 1365-3083 | - |
dc.identifier.isi | WOS:000255725000004 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.citeulike | 2797894 | - |
dc.identifier.issnl | 0300-9475 | - |