ArticleThe Journal of investigative dermatology2009
Bcl-3 acts as an innate immune modulator by controlling antimicrobial responses in keratinocytes.
Article in The Journal of investigative dermatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 31 citations in OpenAlex.
- Sea lice (Frontiers in genetics · 2025Article
- Innate Antiviral Immunity in the Skin.Trends in immunology · 2018Review
- Shh and p50/Bcl3 signaling crosstalk drives pathogenesis of BCCs in Gorlin syndrome.Oncotarget · 2015Article
- The NF-κB regulator Bcl-3 modulates inflammation during contact hypersensitivity reactions in radioresistant cells.European journal of immunology · 2015Article
- Cathelicidin antimicrobial peptide LL-37 in psoriasis enables keratinocyte reactivity against TLR9 ligands.The Journal of investigative dermatology · 2012Article
- Regulation of cathelicidin antimicrobial peptide expression by an endoplasmic reticulum (ER) stress signaling, vitamin D receptor-independent pathway.The Journal of biological chemistry · 2011Article
- The IκB family member Bcl-3 coordinates the pulmonary defense against Klebsiella pneumoniae infection.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- The vitamin D-antimicrobial peptide pathway and its role in protection against infection.Future microbiology · 2009Review
- Atopic dermatitis and vitamin D: facts and controversies.Anais brasileiros de dermatologiaReview
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Innate immune responses involve the production of antimicrobial peptides (AMPs), chemokines, and cytokines. We report here the identification of B-cell leukemia (Bcl)-3 as a modulator of innate immune signaling in keratinocytes. In this study, it is shown that Bcl-3 is inducible by the Th2 cytokines IL-4 and IL-13 and is overexpressed in lesional skin of atopic dermatitis (AD) patients. Bcl-3 was shown to be important to cutaneous innate immune responses as silencing of Bcl-3 by small-interfering RNA (siRNA) reversed the downregulatory effect of IL-4 on the HBD3 expression. Bcl-3 silencing enhanced vitamin D3 (1,25D3)-induced gene expression of cathelicidin AMP in keratinocytes, suggesting a negative regulatory function on cathelicidin transcription. Furthermore, 1,25D3 suppressed Bcl-3 expression in vitro and in vivo. This study identified Bcl-3 as an important modulator of cutaneous innate immune responses and its possible therapeutic role in AD.
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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.