2007
DOI: 10.1111/j.1398-9995.2007.01580.x
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Selective blockade of NF‐κB by novel mutated IκBα suppresses CD3/CD28‐induced activation of memory CD4+ T cells in asthma

Abstract: IkappaBalphaM might be beneficial to augment memory CD4(+) T-cell tolerance through modulating B7-CD28/CTLA-4 co-stimulatory pathways and NF-kappaB-dependent cytokine profiles in allergic inflammatory diseases including asthma.

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Cited by 17 publications
(13 citation statements)
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“…NF-κB-mediated expression of Th2 cytokines and chemokines drives recruitment and infiltration of eosinophils in allergic asthma (29,37,38). Club cells have recently been identified as the principal source of Figure 1.…”
Section: Introductionmentioning
confidence: 99%
“…NF-κB-mediated expression of Th2 cytokines and chemokines drives recruitment and infiltration of eosinophils in allergic asthma (29,37,38). Club cells have recently been identified as the principal source of Figure 1.…”
Section: Introductionmentioning
confidence: 99%
“…Nuclear proteins were extracted and gel shift assay was conducted as described previously 3. Apparently increased NF-κB activity was detected in the mass relative to that in the normal trachea (figure 2), demonstrating a potential role for NF-κB in the pathogenesis of RDD.…”
Section: Case Reportmentioning
confidence: 90%
“…Extranodal involvement including the skin, orbit and nasopharynx occurs in approximately one-third of patients 2. Overactivity of nuclear factor κB (NF-κB, p50/p65) is linked with inflammatory, cancerous and autoimmune diseases 3. We describe an uncommon case of life-threatening RDD of the trachea in association with NF-κB overactivity.…”
mentioning
confidence: 96%
“…Targeted NF-ĸB suppression contributes to memory Th2 cell tolerance through modulating B7-CD28/cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) costimulatory pathways and NF-ĸB-dependent cytokine profiles in asthma [62]. Interestingly, selective blockade of NF-ĸB by mutated IĸBα still results in maturation and T cell priming activity of DCs due to an alternative pathway of NF-ĸB activation, which is at least mediated by binding lymphotoxin β receptor and presenting p100/RelB dimers [63].…”
Section: Tslp and Nf-ĸb Crosstalk In Asthma And Allergymentioning
confidence: 99%