ArticleImmunology1998
Lymphotoxin-alpha is an important autocrine factor for CD40 + interleukin-4-mediated B-cell activation in normal and atopic donors.
Article in Immunology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 22 citations in OpenAlex.
- Increased local cytokine production at culprit superficial femoral artery plaques.Journal of thrombosis and thrombolysis · 2013Trial
- Distinct roles for B cell-derived LTα3 and LTα1β2 in TNF-mediated ileitis.Nature immunology · 2025Article
- Direct and indirect regulation of cytokine and cell cycle proteins by EBNA-2 during Epstein-Barr virus infection.Journal of virology · 2001Article
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Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stimulation of human B cells with anti-CD40 + interleukin-4 (IL-4) results not only in proliferation and immunoglobulin E (IgE)-production, but also increased production of the cytokine lymphotoxin-alpha (LT-alpha) (formerly also known as tumour necrosis factor-beta (TNF-beta)). Here, we studied the role of LT-alpha (TNF-beta) in B cells following stimulation with anti-CD40 + IL-4 from normal versus atopic donors. Anti-CD40 + IL-4 stimulation of peripheral blood mononuclear cells (PBMC) from atopic donors resulted in enhanced production of soluble LT-alpha (TNF-beta) and increased membrane LT-alpha (TNF-beta) expression on the B cells compared with normal donors. Functional evaluation of LT-alpha (TNF-beta) in CD40 + IL-4-stimulated B cells shows that recombinant LT-alpha (TNF-beta) induces proliferation of B cells and enhances CD40 + IL-4-mediated B-cell proliferation and IgE synthesis in both normal and atopic donors in a dose-dependent manner. These findings were supported by semiquantitative analysis of epsilon-germline transcripts using reverse transcription-polymerase chain reaction (RT-PCR) showing increased epsilon-germline transcription in the presence of LT-alpha. Furthermore, addition of anti-LT-alpha (anti-TNF-beta) to CD40 + IL-4-stimulated B cells partially inhibited proliferation and IgE synthesis in a dose-dependent manner indicating a role of endogenous LT-alpha (TNF-beta) production by B cells during continued CD40 + IL-4 stimulation. These data suggest that LT-alpha (TNF-beta) plays a potentially significant role during B-cell proliferation and IgE synthesis. Moreover, LT-alpha (TNF-beta) production seems to be differentially regulated in B cells from normal and atopic donors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.