Induction of the nuclear IκB protein IκB-ζ upon stimulation of B cell antigen receptor

Hijioka, Kuniaki; Matsuo, Susumu; Eto-Kimura, Akiko; Takeshige, Koichiro; Muta, Tsuyoshi

doi:10.1016/j.bbrc.2007.03.002

Cited by 7 publications

(7 citation statements)

References 23 publications

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“…Of note, IκBζ also participates in the regulation of adaptive immunity. For example, IκBζ expression is robustly induced in mouse B‐lymphoma A20 cells upon treatment with B‐cell antigen receptor . In addition, the overexpression of IκBζ together with retinoic acid‐related orphan receptor α/γ promotes the differentiation of naive CD4 + T cells into Th17 cells .…”

Section: Blockade Of Iκbζ Translationmentioning

confidence: 99%

“…For example, IjBf expression is robustly induced in mouse B-lymphoma A20 cells upon treatment with B-cell antigen receptor. 48 In addition, the overexpression of IjBf together with retinoic acid-related orphan receptor a/c promotes the differentiation of naive CD4 + T cells into Th17 cells. 49 These observations suggest that IjBf is an essential driver of inflammatory and immune responses.…”

Section: Blockade Of Ijbf Translationmentioning

confidence: 99%

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Itaconate: an emerging determinant of inflammation in activated macrophages

Zhang

Zheng

et al. 2018

Immunol Cell Biol

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Macrophages play a central role in innate immunity as the first line of defense against pathogen infection. Upon exposure to inflammatory stimuli, macrophages rapidly respond and subsequently undergo metabolic reprogramming to substantially produce cellular metabolites such as itaconate. As a derivate of the tricarboxylic acid cycle, itaconate is derived from the decarboxylation of cis‐aconitate mediated by immunoresponsive gene 1 in the mitochondrial matrix. It is well known that itaconate has a direct antimicrobial effect by inhibiting isocitrate lyase. Strikingly, two recent studies published in Nature showed that itaconate markedly decreases the production of proinflammatory mediators in lipopolysaccharide‐treated macrophages and ameliorates sepsis and psoriasis in animal models, revealing a novel biological action of itaconate beyond its regular roles in antimicrobial defense. The mechanism for this anti‐inflammatory effect has been proposed to involve the inhibition of succinate dehydrogenase, blockade of IκBζ translation and activation of Nrf2. These intriguing discoveries provide a new explanation for how macrophages are switched from a pro‐ to an anti‐inflammatory state to limit the damage and facilitate tissue repair under proinflammatory conditions. Thus, the emerging effect of itaconate as a crucial determinant of macrophage inflammation has important implications in further understanding cellular immunometabolism and developing future therapeutics for the treatment of inflammatory diseases. In this review, we focus on the roles of itaconate in controlling the inflammatory response during macrophage activation, providing a rationale for future investigation and therapeutic intervention.

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Section: Blockade Of Iκbζ Translationmentioning

confidence: 99%

Section: Blockade Of Ijbf Translationmentioning

confidence: 99%

Itaconate: an emerging determinant of inflammation in activated macrophages

Zhang

Zheng

et al. 2018

Immunol Cell Biol

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“…The important and selective role of IκB-ζ is demonstrated by the fact that IκB-ζ -deficient splenocytes exhibit defective proliferation in response to LPS [51]. This strongly suggests that B cells have the capacity to induce IκB-ζ and that the induced IκB-ζ plays an essential role in the LPS-mediated proliferation of B cells [56]. Since IL-6 is produced by antigen- or mitogen-stimulated B cells, IκB-ζ may be involved in the induction of IL-6 and therefore, in B-cell differentiation and haematopoietic cell growth [53].…”

Section: Nuclear Regulation Of Nf-κbmentioning

confidence: 99%

NF‐κB regulation: the nuclear response

Mankan

Lawless

Gray

et al. 2009

J Cellular Molecular Medi

155

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Nuclear factor κB (NF-κB) is an inducible transcription factor that tightly regulates the expression of a large cohort of genes. As a key component of the cellular machinery NF-κB is involved in a wide range of biological processes including innate and adaptive immunity, inflammation, cellular stress responses, cell adhesion, apoptosis and proliferation. Appropriate regulation of NF-κB is critical for the proper function and survival of the cell. Aberrant NF-κB activity has now been implicated in the pathogenesis of several diseases ranging from inflammatory bowel disease to autoimmune conditions such as rheumatoid arthritis. Systems governing NF-κB activity are complex and there is an increased understanding of the importance of nuclear events in regulating NF-κB's activities as a transcription factor. A number of novel nuclear regulators of NF-κB such as IκB-ζ and PDZ and LIM domain 2 (PDLIM2) have now been identified, adding another layer to the mechanics of NF-κB regulation. Further insight into the functions of these molecules raises the prospect for better understanding and rational design of therapeutics for several important diseases.

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“…The expression of IκBζ is induced upon B cell stimulation via the B cell receptor (BCR), TLR7 or TLR9, whereat the BCR and TLRs act synergistically [35,89]. Furthermore, IκBζ signalling in B cells is essential for TLR-induced but not BCR-induced Il10 and Ctla4 gene induction as well as B cell proliferation.…”

Section: Iκbζ In Adaptive Immunitymentioning

confidence: 99%

Atypical IκB proteins in immune cell differentiation and function

et al. 2016

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The NF-κB/Rel signalling pathway plays a crucial role in numerous biological processes, including innate and adaptive immunity. NF-κB is a family of transcription factors, whose activity is regulated by the inhibitors of NF-κB (IκB). The IκB proteins comprise two distinct groups, the classical (cytoplasmic) and the atypical (nuclear) IκB proteins. Although the cytoplasmic regulation of NF-κB is well characterised, its nuclear regulation mechanisms remain marginally elucidated. However, work from recent years indicated that nuclear IκBs contribute significantly to the modulation of NF-κB-mediated transcription in the immune system. Here, we discuss the role of the atypical IκB proteins Bcl-3, IκBζ, IκBNS, IκBη and IκBL for the regulation of gene expression and effector functions in immune cells.

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Induction of the nuclear IκB protein IκB-ζ upon stimulation of B cell antigen receptor

Cited by 7 publications

References 23 publications

Itaconate: an emerging determinant of inflammation in activated macrophages

Itaconate: an emerging determinant of inflammation in activated macrophages

NF‐κB regulation: the nuclear response

Atypical IκB proteins in immune cell differentiation and function

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