An Immunohistochemical Analysis of Cytokine Expression in Allergic and Irritant Contact Dermatitis: Investigative Report

Ulfgren, Ann‐Kristin; Klareskog, Lars; Lindberg, Magnus

doi:10.1080/000155500750042899

Cited by 40 publications

(4 citation statements)

References 10 publications

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“…Tr1 clones secreting IL-10 have been isolated from PBMCs in Ni-allergic and nonallergic individuals [12]. IL-10 has been found both in dermal lymphocytes during ongoing allergic reaction [22, 35], and in Ni-specific T-cell clones derived from allergic skin lesions [12]. This indicates that IL-10 is likely to be important in Ni allergy.…”

Section: Discussionmentioning

confidence: 99%

Cytokine Production, Lymphocyte Proliferation and T-Cell Receptor Vβ Expression in Primary Peripheral Blood Mononuclear Cell Cultures from Nickel-Allergic Individuals

Cederbrant

Anderson

Andersson

et al. 2003

Int Arch Allergy Immunol

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Background: Clinical history and patch test constitute the two cornerstones in the diagnosis of nickel (Ni) allergy. Due to technical and interpretative limits of the patch test, the in vitro lymphocyte transformation test (LTT) has been developed for confirming contact allergy; however, most studies show an overlap in lymphocyte proliferation between Ni-allergic and nonallergic subjects using the LTT. The aim of this study was to see if the secretion of cytokines, especially interleukin (IL)-10 and IL-17, or the use of T-cell receptor (TCR) Vβ families in Ni-stimulated primary peripheral blood mononuclear cell (PBMC) cultures might be more useful for discriminating between allergic and nonallergic subjects. Methods: Ni²⁺-stimulated primary PBMC cultures derived from female subjects diagnosed as Ni-allergic (n = 5) or nonallergic (n = 5) on the basis of a positive or negative patch test were assessed for cell proliferation by tritiated thymidine incorporation and for production of interferon-γ, IL-4, IL-10 and IL-17 in the culture supernatant by ELISA. The immunophenotype and TCR-Vβ family affiliation of the Ni²⁺-induced lymphoblasts were determined by flow cytometry. Results: Lymphocytes from Ni-allergic individuals challenged with a high and a low concentration of Ni showed significantly higher cell proliferation than lymphocytes from nonallergic individuals, but all subjects showed a positive LTT result (stimulation index >2). We found a significantly higher release of IL-10 in Ni²⁺-treated cultures from Ni-allergic compared with nonallergic subjects that provided better separation between individuals in the two groups than did lymphocyte proliferation. The proliferating lymphoblasts were predominantly CD4+, and in 2 of the 5 Ni-allergic subjects, but in none of the 5 nonallergic subjects, the CD4+ lymphoblasts showed a dominance of TCR-Vβ17. Conclusions: Determination of IL-10 production in primary PBMC cultures is a potentially promising in vitro method for discrimination of Ni allergy in females, as compared with cell proliferation.

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Section: Discussionmentioning

confidence: 99%

Cytokine Production, Lymphocyte Proliferation and T-Cell Receptor Vβ Expression in Primary Peripheral Blood Mononuclear Cell Cultures from Nickel-Allergic Individuals

Cederbrant

Anderson

Andersson

et al. 2003

Int Arch Allergy Immunol

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“…Immunohistochemical analyses are a useful research method because they enable localization of specific active antigens by use of targeted antibodies, thus providing additional information on individual diseases, including CD. In addition to diagnostic purposes, immunohistochemistry is also used in scientific research, helping us gain a better insight into the distribution and localization of biomarkers and expressions of individual proteins in various tissues ( 30 - 32 ).…”

Section: Immunohistochemistry Of Contact Dermatitis Skin Lesionsmentioning

confidence: 99%

Irritant and Allergic Contact Dermatitis – Skin Lesion Characteristics

Novak-Bilić

Vučić

Japundžić

et al. 2018

ACC

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SUMMARY – Contact skin lesions may be the consequences of contact with various irritants or allergens, or due to other factors (e.g., UV radiation, microbials), intrinsic factors (e.g., in autoimmune responses), or even their combination. There are many substances related to irritant contact dermatitis (CD), causing irritant or toxic effects, e.g., chemical and physical agents, plants, phototoxic agents, airborne irritants, etc. Impaired barrier function (e.g., aberrancies in epidermal pH buffering capabilities) also participates by promoting bacterial biofilms and creating an environment favoring sensitization. Development of allergic CD skin lesions includes complex immune pathways and inflammatory mediators, influenced by both genetic (predominantly filaggrin mutations) and environmental triggers. In the pathogenesis of allergic CD, antimicrobial peptides play a prominent role; they are produced by various skin cells (e.g., keratinocytes, sebocytes) and move to inflamed lesions during an inflammation process. Also, in allergic CD skin lesions, the skin shows different types of immune responses to individual allergens, although clinical manifestations do not depend on the causative allergen type, e.g., nickel stimulates immune activation primarily of the Th1/Th17 and Th22 components. Also important are alarmins, proteases, immunoproteomes, lipids, natural moisturizing factors, tight junctions, smoking, etc. We expect that future perspectives may reveal new pathogenetic factors and scientific data important for the workup and treatment of patients with CD.

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“… 37 Accordingly, only few IL‐1β‐expressing cells were previously detected in lesional skin of allergic and irritant contact dermatitis, and these did not change over time (6 to 72 h). 38 However, it should be noted that only upper epidermal layers were examined in our study and dermal cytokine concentrations were not assessed.…”

Section: Discussionmentioning

confidence: 99%

Topical inflammasome inhibition with disulfiram prevents irritant contact dermatitis

Bonnekoh

Vera

Abad-Perez

et al. 2021

Clinical & Translational All

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Background:The pathogenesis of contact dermatitis, a common inflammatory skin disease with limited treatment options, is held to be driven by inflammasome activation induced by allergens and irritants. We here aim to identify inflammasometargeting treatment strategies for irritant contact dermatitis. Methods:A high content screen with 41,184 small molecules was performed using fluorescent Apoptosis associated speck-like protein containing a CARD (ASC) speck formation as a readout for inflammasome activation. Hit compounds were validated for inhibition of interleukin (IL)-1β secretion. Of these, the approved thiuramdisulfide derivative disulfiram was selected and tested in a patch test model of irritant contact dermatitis in 25 healthy volunteers. Topical application of disulfiram, mometasone or vehicle was followed by application of sodiumdodecylsulfate (SDS) for 24 h each. Eczema induction was quantified by mexameter and laser speckle imaging. Corneocyte sampling of lesional skin was performed to assess inflammasome-mediated cytokines IL-1β and IL-18.Results: Disulfiram induced a dose-dependent inhibition of ASC speck formation and IL-1β release in cellular assays in vitro. In vivo, treatment with disulfiram, but not with vehicle and less mometasone, inhibited SDS-induced eczema. This was demonstrated by significantly lower erythema and total perfusion values assessed by mexameter and laser speckle imaging for disulfiram compared to vehicle (p < 0.001) and/or mometasone (p < 0.001). Also, corneocyte IL-18 levels were significantly reduced after application of disulfiram compared to vehicle (p < 0.001). Conclusion:We show that disulfiram is a dose-dependent inhibitor of inflammasome pathway activation in vitro and inhibitor of SDS-induced eczema in vivo.Topical application of disulfiram represents a potential treatment option for irritant contact dermatitis.This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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An Immunohistochemical Analysis of Cytokine Expression in Allergic and Irritant Contact Dermatitis: Investigative Report

Cited by 40 publications

References 10 publications

Cytokine Production, Lymphocyte Proliferation and T-Cell Receptor Vβ Expression in Primary Peripheral Blood Mononuclear Cell Cultures from Nickel-Allergic Individuals

Cytokine Production, Lymphocyte Proliferation and T-Cell Receptor Vβ Expression in Primary Peripheral Blood Mononuclear Cell Cultures from Nickel-Allergic Individuals

Irritant and Allergic Contact Dermatitis – Skin Lesion Characteristics

Topical inflammasome inhibition with disulfiram prevents irritant contact dermatitis

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