TRIF signaling is essential for TLR4-driven IgE class switching (IRM5P.707)
العنوان: | TRIF signaling is essential for TLR4-driven IgE class switching (IRM5P.707) |
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المؤلفون: | Erin Janssen, Esra Ozcan, Kyriaki Liadaki, Haifa Jabara, John Manis, Sumana Ullas, Shizuo Akira, Katherine Fitzgerald, Douglas Golenbock, Raif Geha |
المصدر: | The Journal of Immunology. 192:62.8-62.8 |
بيانات النشر: | The American Association of Immunologists, 2014. |
سنة النشر: | 2014 |
مصطلحات موضوعية: | Immunology, Immunology and Allergy |
الوصف: | The TLR4 ligand LPS causes mouse B cells to undergo IgE and IgG1 isotype switching in the presence of IL-4. TLR4 activates two signaling pathways mediated by the adaptor molecules MyD88 and TRAM, which recruits TRIF. Following stimulation with LPS+IL-4, Tram-/- and Trif-/- B cells completely failed to express Cε germ line transcripts (GLT) and secrete IgE. In contrast, Myd88-/- B cells had normal expression of Cγ1 GLT, but reduced IgE secretion in response to LPS+IL-4. Following LPS+IL-4 stimulation, Cγ1 GLT expression was modestly reduced in Tram-/- and Trif-/- B cells, whereas Aicda expression and IgG1 secretion were reduced in Tram-/-,Trif-/-, and Myd88-/- B cells. B cells from all strains secreted normal amounts of IgE and IgG1 in response to anti-CD40+IL-4. Following stimulation with LPS+IL-4, Trif-/- B cells failed to sustain NFκB p65 nuclear translocation beyond 3 hours and had reduced binding of p65 to the Iε promoter. Addition of the NFκB inhibitor, JSH-23, to wild-type B cells 15 hours after LPS+IL-4 stimulation selectively blocked Cε GLT expression and IgE secretion, but had little effect on Cγ1 GLT expression and IgG secretion. These results indicate that sustained activation of NFκB driven by TRIF is essential for LPS+IL-4 driven activation of the Cε locus and class switching to IgE. |
تدمد: | 1550-6606 0022-1767 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_________::8968ec250489de5b6d223de51b1e5522 https://doi.org/10.4049/jimmunol.192.supp.62.8 |
رقم الأكسشن: | edsair.doi...........8968ec250489de5b6d223de51b1e5522 |
قاعدة البيانات: | OpenAIRE |
تدمد: | 15506606 00221767 |
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