دورية أكاديمية
Cross-talk between TLR4 and FcgammaReceptorIII (CD16) pathways.
| العنوان: | Cross-talk between TLR4 and FcgammaReceptorIII (CD16) pathways. |
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| المؤلفون: | Daniel Rittirsch, Michael A Flierl, Danielle E Day, Brian A Nadeau, Firas S Zetoune, J Vidya Sarma, Clement M Werner, Guido A Wanner, Hans-Peter Simmen, Markus S Huber-Lang, Peter A Ward |
| المصدر: | PLoS Pathogens, Vol 5, Iss 6, p e1000464 (2009) |
| بيانات النشر: | Public Library of Science (PLoS), 2009. |
| سنة النشر: | 2009 |
| المجموعة: | LCC:Immunologic diseases. Allergy LCC:Biology (General) |
| مصطلحات موضوعية: | Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5 |
| الوصف: | Pathogen-pattern-recognition by Toll-like receptors (TLRs) and pathogen clearance after immune complex formation via engagement with Fc receptors (FcRs) represent central mechanisms that trigger the immune and inflammatory responses. In the present study, a linkage between TLR4 and FcgammaR was evaluated in vitro and in vivo. Most strikingly, in vitro activation of phagocytes by IgG immune complexes (IgGIC) resulted in an association of TLR4 with FcgammaRIII (CD16) based on co-immunoprecipitation analyses. Neutrophils and macrophages from TLR4 mutant (mut) mice were unresponsive to either lipopolysaccharide (LPS) or IgGIC in vitro, as determined by cytokine production. This phenomenon was accompanied by the inability to phosphorylate tyrosine residues within immunoreceptor tyrosine-based activation motifs (ITAMs) of the FcRgamma-subunit. To transfer these findings in vivo, two different models of acute lung injury (ALI) induced by intratracheal administration of either LPS or IgGIC were employed. As expected, LPS-induced ALI was abolished in TLR4 mut and TLR4(-/-) mice. Unexpectedly, TLR4 mut and TLR4(-/-) mice were also resistant to development of ALI following IgGIC deposition in the lungs. In conclusion, our findings suggest that TLR4 and FcgammaRIII pathways are structurally and functionally connected at the receptor level and that TLR4 is indispensable for FcgammaRIII signaling via FcRgamma-subunit activation. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1553-7366 1553-7374 95535268 |
| العلاقة: | http://europepmc.org/articles/PMC2685003?pdf=renderTest; https://doaj.org/toc/1553-7366Test; https://doaj.org/toc/1553-7374Test |
| DOI: | 10.1371/journal.ppat.1000464 |
| الوصول الحر: | https://doaj.org/article/d667dbf35ae5439f9553526899f07d07Test |
| رقم الانضمام: | edsdoj.667dbf35ae5439f9553526899f07d07 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 15537366 15537374 95535268 |
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| DOI: | 10.1371/journal.ppat.1000464 |