ArticleJournal of immunology (Baltimore, Md. : 1950)2014
TRIF signaling is essential for TLR4-driven IgE class switching.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Decoding Allergic Conjunctivitis: Latest Perspectives on Etiological Drivers and Immunopathological Mechanisms.Clinical reviews in allergy & immunology · 2025Review
- T cell independent antibody responses with class switch and memory using peptides anchored on liposomes.NPJ vaccines · 2024Article
- B cells mediate lung ischemia/reperfusion injury by recruiting classical monocytes via synergistic B cell receptor/TLR4 signaling.The Journal of clinical investigation · 2024Article
- Epicutaneous Staphylococcus aureus induces IL-36 to enhance IgE production and ensuing allergic disease.The Journal of clinical investigation · 2021Article
- Birch Pollen Induces Toll-Like Receptor 4-Dependent Dendritic Cell Activation Favoring T Cell Responses.Frontiers in allergy · 2021Article
- Cutaneous Exposure to Clinically Relevant Lone Star Ticks Promotes IgE Production and Hypersensitivity through CD4Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Clinical observation of ulinastatin combined with CRRT in the treatment of early cardiopulmonary resuscitation.Experimental and therapeutic medicine · 2017Article
- The Role of TLR4 on B Cell Activation and Anti-Journal of immunology research · 2016Review
- Three conserved MyD88-recruiting TLR residues exert different effects on the human TLR4 signaling pathway.Immunologic research · 2015Article
- Differences in PGE2 production between primary human monocytes and differentiated macrophages: role of IL-1β and TRIF/IRF3.PloS one · 2014Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
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 Toll/IL-IR domain-containing adapter-inducing IFN-β (TRIF)-related adaptor molecule (TRAM), which recruits TRIF. Following stimulation with LPS plus IL-4, Tram(-/-) and Trif(-/-) B cells completely failed to express Cε germline transcripts (GLT) and secrete IgE. In contrast, Myd88(-/-) B cells had normal expression of Cε GLT but reduced IgE secretion in response to LPS plus IL-4. Following LPS plus 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 plus IL-4. Following stimulation with LPS plus IL-4, Trif(-/-) B cells failed to sustain NF-κB p65 nuclear translocation beyond 3 h and had reduced binding of p65 to the Iε promoter. Addition of the NF-κB inhibitor, JSH-23, to wild-type B cells 15 h after LPS plus 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 NF-κB driven by TRIF is essential for LPS plus IL-4-driven activation of the Cε locus and class switching to IgE.
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