ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
Increased IkappaB alpha expression is essential for the tolerogenic property of TGF-beta-exposed APCs.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
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- AIMP1: multifunctional regulator in physiology and pathology with therapeutic implications.PeerJ · 2025Review
- Transforming Growth Factor-Beta (TGF-β) Signaling in Cancer-A Betrayal Within.Frontiers in pharmacology · 2022Review
- Intranasal Delivery: Effects on the Neuroimmune Axes and Treatment of Neuroinflammation.Pharmaceutics · 2020Review
- Sjögren's syndrome-associated microRNAs in CD14(+) monocytes unveils targeted TGFβ signaling.Arthritis research & therapy · 2016Article
- Astrocytic TGF-β signaling limits inflammation and reduces neuronal damage during central nervous system Toxoplasma infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Complex temporal changes in TGFβ oncogenic signaling drive thyroid carcinogenesis in a mouse model.Carcinogenesis · 2013Article
- TGF-β induces miR-182 to sustain NF-κB activation in glioma subsets.The Journal of clinical investigation · 2012Article
- Inhibition of proinflammatory RANTES expression by TGF-beta1 is mediated by glycogen synthase kinase-3beta-dependent beta-catenin signaling.The Journal of biological chemistry · 2011Article
- Intranasal delivery systems for traumatic brain injury: Advancements and perspectives.Journal of tissue engineeringReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
IkappaB alpha is an inhibitor of the transcriptional factor NF-kappaB, and it is an essential component of the signaling pathways that lead to expression of inflammatory molecules. These include cytokines and costimulatory molecules associated with antigen presentation in an inflammatory immune response. In this study, we report that antigen-presenting cells exposed to TGF-beta induce peripheral tolerance by increasing IkappaB alpha expression. Exposure of antigen presenting cells (APCs) to TGF-beta is known to impair their ability to secrete IL-12, and such impairment correlated with reduced NF-kappaB activity as indicated by significantly reduced nuclear levels of p50, an essential subunit of NF-kappaB for IL-12 transcription. Blockade of increased nuclear IkappaB alpha in APCs by expression of small interfering RNA molecules (siRNAs) targeting IkappaB alpha transcripts prevented IL-12 impairment and the decline in nuclear p50 levels. Furthermore, such IkappaB alpha blockade also interfered with the tolerogenic property of TGF-beta-exposed APCs. However, increased expression of IkappaB alpha in APCs, independent of TGF-beta exposure, reduced nuclear p50 levels and permitted tolerance induction by APCs. Thus, our findings attribute a direct and significant role to IkappaB alpha in the tolerogenic potential of APCs. Increased IkappaB alpha expression in APCs may therefore offer a therapeutic approach to achieve antigen-specific immunomodulation.
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What OpenQuestion holds
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.