Publications by authors named "I V Afonina"
Rare mutations in CARD14 promote psoriasis by inducing CARD14-BCL10-MALT1 complexes that activate NF-κB and MAP kinases. Here, the downstream signalling mechanism of the highly penetrant CARD14E138A alteration is described. In addition to BCL10 and MALT1, CARD14E138A associated with several proteins important in innate immune signalling.
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- CARD14 is a protein that plays a key role in activating NF-ĸB signaling and inflammatory gene expression in skin cells, and mutations in CARD14 are linked to psoriasis and other skin conditions.
- Research using affinity purification and mass spectrometry identified polo-like kinase 1 (PLK1) as a new binding partner of CARD14, connecting through a specific region rather than its known CARD domain.
- The psoriasis-related CARD14(E138A) variant recruits PLK1 to signaling complexes in skin cells and altering this binding site enhances inflammatory signaling, suggesting that PLK1 serves as a negative regulator in CARD14’s activity.
Linear ubiquitination is an important post-translational modification regulating the activation of numerous proinflammatory signalling mediators. Deregulated linear ubiquitination has been implicated in the pathogenesis of several inflammatory and autoimmune diseases. In this issue, Miao et al.
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- IL-33 is crucial in allergic diseases like asthma, primarily promoting type 2 immune responses, but it can also drive type 1 responses.
- The study focused on how A20 regulates IL-33 signaling in macrophages and lung immunity in mice lacking A20 in myeloid cells.
- Results showed that without A20, there was reduced type 2 immune response and increased type 1 signaling, leading to IFN-γ production, indicating A20's role as a negative regulator of IL-33-induced immune responses.
Immune checkpoint blockade (ICB) has heralded a new era in cancer therapy. Research into the mechanisms underlying response to ICB has predominantly focused on T cells; however, effective immune responses require tightly regulated crosstalk between innate and adaptive immune cells. Here, we combine unbiased analysis of blood and tumors from metastatic breast cancer patients treated with ICB with mechanistic studies in mouse models of breast cancer.
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