The role of interleukin‐<scp>1β</scp> in the immune response to contact allergens

Yeung, Kelvin; Mraz, Veronika; Geisler, Carsten; Skov, Lone; Bonefeld, Charlotte M.

doi:10.1111/cod.13955

Cited by 23 publications

(13 citation statements)

References 83 publications

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“…Furthermore, IL-1 β , IL-6, and TNF- α , critical proinflammatory factors, are involved in the activation of immune cells and regulation of the inflammatory response. 48 Accordingly, we found that the expression of IL-1 β , IL-6, and TNF- α was reduced after METTL3 inhibition. Similarly, silencing METTL3 in dental pulp inflammation suppressed the NF-κB signaling pathway and reduced the expression of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 74%

Inhibition of the m6A Methyltransferase METTL3 Attenuates the Inflammatory Response inFusarium solani-Induced Keratitis via the NF-κB Signaling Pathway

Tang

Huang

2022

Invest. Ophthalmol. Vis. Sci.

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Purpose The purpose of this study was to elucidate the effect of methyltransferase-like enzyme 3 (METTL3) on inflammation and the NF-κB signaling pathway in fungal keratitis (FK). Methods We established corneal stromal cell models and FK mouse models by incubation with Fusarium solani . The overall RNA N6-methyladenosine (m6A) level was determined using an m6A RNA methylation assay kit. The expression of METTL3 was quantified via real-time quantitative polymerase chain reaction (RT–PCR), Western blotting, and immunofluorescence. Subsequently, the level of tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) was identified by Western blotting and immunofluorescence. Moreover, we assessed the effect of METTL3 by transfecting cells with siRNA (in vitro) or adeno-associated virus (in vivo). Hematoxylin and eosin (H&E) staining and slit-lamp biomicroscopy were performed to evaluate corneal damage. Furthermore, the state of NF-κB signaling pathway activation was examined by Western blotting. In addition, RT–PCR and enzyme-linked immunosorbent assays (ELISAs) were performed to evaluate levels of the pro-inflammatory factors interleukin-1 β (IL-1 β ), interleukin-6 (IL-6) and TNF- ɑ . Results Our data demonstrated that the levels of the RNA m6A methylation and METTL3 were dramatically increased and that the NF-κB signaling pathway was activated in Fusarium solani -induced keratitis. Inhibition of METTL3 decreased the level of TRAF6, downregulated the phospho-p65(p-p65)/p65 and phospho-IκB(p-IκB)/IκB protein ratios, simultaneously attenuating the inflammatory response and fungal burden in FK. Conclusions Our research suggests that the m6A methyltransferase METTL3 regulates the inflammatory response in FK by modulating the NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 74%

Inhibition of the m6A Methyltransferase METTL3 Attenuates the Inflammatory Response inFusarium solani-Induced Keratitis via the NF-κB Signaling Pathway

Tang

Huang

2022

Invest. Ophthalmol. Vis. Sci.

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“…In this state, IgE+ LCs are present in the middle to upper layers of the epidermis, and IgE+ IDECs are present in the subepidermal layer of the epidermis in order to capture allergens that penetrate skin with an impaired barrier function, and IgE+ LCs primarily react to these allergens ( Figure 4 b: outer parts). In addition to the state of chronic inflammatory skin lesion, introduction of various inducing factors, such as increased specific-allergen exposure, innate immune danger signals (e.g., danger-associated molecular patters and pathogen-associated molecular patterns) resulting from skin barrier disruption and/or pathogen provocation, and release of proinflammatory cytokines (IL-1α, IL-1β, IL-18, and TNF-α) [ 7 , 47 , 105 , 106 ], can result in spongiosis dermatitis as an acute lesion in lichenified eczema. This is caused by the aforementioned pathomechanism, i.e., induction of keratinocyte apoptosis by the interaction between activated IgE+ LCs and accumulated IgE+ IDECs that captured allergens such as HDMs, the Fas/FasL system stimulated by INF-γ secreted by activated CD4+ T cells, and perforin and granzyme B released by activated CD4+ and CD8+ T cells ( Figure 4 b: central part).…”

Section: Pathomechanism Of Eczematous Dermatitis In Ad As Allergic In...mentioning

confidence: 99%

Immunological Pathomechanisms of Spongiotic Dermatitis in Skin Lesions of Atopic Dermatitis

Tanei

Hasegawa

2022

IJMS

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Atopic dermatitis (AD) is a chronic pruritic skin disease with a complex pathogenesis underlying its heterogeneous clinical phenotypes and endotypes. The skin manifestation of AD reflects the cytokine milieu of a type-2-dominant immunity axis induced by genetic predisposition, innate immunity dysregulation, epidermal barrier defects, and allergic inflammation. However, the detailed pathomechanism of eczematous dermatitis, which is the principal characteristic of AD, remains unclear. This review examines previous studies demonstrating research progress in this area and considers the immunological pathomechanism of “spongiotic dermatitis”, which is the histopathological hallmark of eczematous dermatitis. Studies in this field have revealed the importance of IgE-mediated delayed-type hypersensitivity, the Fas/Fas-ligand system, and cell-mediated cytotoxicity in inducing the apoptosis of keratinocytes in spongiotic dermatitis. Recent studies have demonstrated that, together with infiltrating CD4 T cells, IgE-expressing dendritic cells (i.e., inflammatory dendritic epidermal cells and Langerhans cells) that capture specific allergens (i.e., house dust mites) are present in the spongiotic epidermis of lichenified eczema in patients with IgE-allergic AD. These findings suggest that IgE-mediated delayed-type hypersensitivity plays a pivotal role in the pathogenesis of spongiotic dermatitis in the skin lesions of AD.

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“…Daug dėmesio IL-1 tyrimams skyrė Bonefeld su kolegomis, kurie pradžioje tyrimus atliko su pelėmis, vėliau ir žmonėmis [34]. Yra tyrimų, kuriuose stebėtas IL-1β koncentracijos padidėjimas alerginio kontaktinio dermatito metu ūminėje fazėje [35,36].…”

Section: Citokinai Alerginio Kontaktinio Dermatito Patogenezėjeunclassified

Kontaktinė alergija sunkiesiems metalams: rizikos veiksniai ir patogeneziniai mechanizmai

Linauskienė

2022

PIA

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Disertacija apginta viešajame gynimo tarybos posėdyje 2022 m. kovo mėn. 24 d. Vilniaus universiteto ligoninėje Santaros klinikų Pulmonologijos ir alergologijos centre.Mokslinis vadovas: prof. dr. Laura Malinauskienė (Vilniaus universitetas, medicinos ir sveikatos mokslai, medicina – M 001).Mokslinė konsultantė: prof. dr. Marléne Isaksson (Lundo universitetas, medicinos ir sveikatos mokslai, medicina – M 001).Gynimo taryba: prof. dr. Rūta Dubakienė (Vilniaus universitetas, medicinos ir sveikatos mokslai, medicina – M 001), prof. dr. Matilda Bylaitė-Bučinskienė (Vilniaus universitetas, medicinos ir sveikatos mokslai, medicina – M 001), dr. Rūta Druteikienė (Fizinių ir technologijos mokslų centras, gamtos mokslai, fizika – N 002), prof. dr. Violeta Kvedarienė (Vilniaus universitetas, medicinos ir sveikatos mokslai, medicina – M 001), prof. dr. Radoslaw Spiewak (Krokuvos Jogailos universitetas, medicinos ir sveikatos mokslai, medicina – M 001).Straipsnyje pateikiami esminiai disertacijos rezultatai.

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The role of interleukin‐1β in the immune response to contact allergens

Cited by 23 publications

References 83 publications

Inhibition of the m6A Methyltransferase METTL3 Attenuates the Inflammatory Response inFusarium solani-Induced Keratitis via the NF-κB Signaling Pathway

Inhibition of the m6A Methyltransferase METTL3 Attenuates the Inflammatory Response inFusarium solani-Induced Keratitis via the NF-κB Signaling Pathway

Immunological Pathomechanisms of Spongiotic Dermatitis in Skin Lesions of Atopic Dermatitis

Kontaktinė alergija sunkiesiems metalams: rizikos veiksniai ir patogeneziniai mechanizmai

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