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1
Kazimirsky, A. N., J. M. Salmasi, G. V. Poryadin, O. A. Svitich, B. G. Bragvadze, A. A. Alekseeva, and L. V. Gankovskaya. "The role of epithelial cells in atopy pathogenesis." Bulletin of Siberian Medicine 18, no. 1 (May 16, 2019): 201–10. http://dx.doi.org/10.20538/1682-0363-2019-1-201-210.
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Aim. The study of the mechanisms of atopic disease formation and a model of immunopathogenesis of the atopic diseases.Methods. Determination of surface lymphocytes receptors in peripheral blood of atopic bronchial asthma and atopic dermatitis patients with the help of monoclonal antibodies using the indirect immunofluorescence method. Expression of genes encoding TLR2, TLR4 and TLR9 receptors of airborne epithelial cells by real-time polymerase chain reaction, as well as determination of cytokine TSLP, IL-33, IL-4 and TGFβ (eBioscience) in airway flushes in atopic asthma patients and healthy people.Results. During the exacerbation of atopic diseases in peripheral blood lymphocytes, an intensive activation process develops with impaired lymphocytes activating apoptosis aimed at the formation of plasma cells capable of developing intensive IgE synthesis. To search for signals that could explain the mechanism of rearrangement of the B-cell part of the immune system during atopy, the epithelium cells of the airways were examined in a group of patients with atopic asthma and found an increase in gene expression coding for TLR2, TLR4, TLR9 in 6, 3 and 2.5 times respectively. Along with increased expression of TLRs genes in patients with bronchial asthma, an increased content of TSLP and IL-33 cytokines secreted by epithelial cells of the airways was detected. These cytokines have an immunoregulatory action - their nearby antigen presenting functions format the Th2 type of immune response, promote the production of cytokines (IL-4, IL-9, IL-13) and cause the development of an allergic type of inflammation.Conclusion. We suppose that the main link in pathogenesis is a disruption of the interaction of TLRs with the corresponding ligands caused by spontaneous dimerization of TLRs under the malonic dialdehyde influence. The intake of slowly metabolized dimers of TLRs into epithelial cells is a signal for genome activation, which leads to the synthesis of allergic cytokines IL-33 and TSLP. Thus, the main immunopathogenesis pathway of atopic diseases is the pathological functional interaction between epithelial cells and peripheral blood B-lymphocytes.
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Brutsche, Martin H., Ingrid Carlen Brutsche, Peter Wood, Nesrin Mogulkoc, Adnan Custovic, Jim Egan, and Ashley Woodcock. "B-cell isotype control in atopy and asthma assessed with cDNA array technology." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (April 1, 2001): L627—L637. http://dx.doi.org/10.1152/ajplung.2001.280.4.l627.
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B-cell isotype switching and the production of IgE is regulated by a variety of gene products through different mechanisms. A better understanding of these processes has the potential to identify markers of disease and new therapeutic targets. The aim of the study was to investigate human B-cell isotype control and IgE production in atopy and asthma with cDNA array technology. Eighteen atopic asthmatic, eight atopic nonasthmatic, and fourteen healthy control subjects were included. Peripheral blood mononuclear cells were separated by gradient centrifugation, mRNA was purified, and the reverse-transcribed probes were hybridized to cDNA membranes. Group differences were assessed with the Mann-Whitney U-test. Twenty-three of seventy-eight tested IgE-related genes had significantly altered expression in atopy and asthma compared with that in the healthy subjects. The differentially expressed genes include surface molecules involved in T- and B-cell interaction and activation, cytokines, intracellular signaling products, and transcription factors. In conclusion, both atopic nonasthmatic and atopic asthmatic individuals had activated proinflammatory pathways, a minimal requirement for B-cell isotype switching, and a clear net pro-IgE cytokine climate.
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Kruglova, L. S., and E. M. Gensler. "Atopic dermatitis: new horizons of therapy." Medical alphabet 1, no. 7 (March 5, 2019): 29–32. http://dx.doi.org/10.33667/2078-5631-2019-1-7(382)-29-32.
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Over the past decades, the first breakthrough milestone in the treatment of severe forms of atopic dermatitis (AD) has been targeted therapy aimed at inhibiting IL-4 and IL-13. This was made possible thanks to advances in the understanding of the pathogenesis of AD, the driver of which is the Th2-type immune response, which also underlies such manifestations of atopy as bronchial asthma, allergic rhinitis, and polynosis. In the case of the Th2-type immune response, cytokines IL-4 and IL-13 are secreted, which are the main promoters of the inflammatory response in AD. Inhibition of IL-4 and IL-13 leads to the prevention of inflammation and is an effective approach to therapy. The use of therapy aimed at inhibition of cytokines allows you to effectively cope with the manifestations of severe and moderately severe blood pressure.
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Ashwi, Shaima, Ahmad Alobaisy, Nawal Herzallah, Fatema Alwaheed, Ibtihal Hadi, Duaa Alabbas, Faisal Al-Rasheed, Nawaf Alshuraym, and Esra Alzein. "Atopic dermatitis in sickle cell children." International Journal Of Community Medicine And Public Health 5, no. 3 (February 24, 2018): 842. http://dx.doi.org/10.18203/2394-6040.ijcmph20180420.
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Sickle cell disease is an autosomal recessive disease characterized by recurrent vaso-occlusive events. Despite the genetic basis of its pathophysiology, recent researchers stated that it is an inflammatory immune-mediated disease where inflammation plays a crucial role in the initiation of adherence between sickle cells and vascular endothelial cells. Allergic, as well as infectious, inflammation is proposed to contribute to the initiation of vaso-occlusive events. Although several researchers reported an association between sickle cell disease and atopic conditions such as bronchial asthma and allergic rhino-conjunctivitis, few cases have reported an association between sickle cell disease and atopic dermatitis. Atopy was reported to be considerably linked to sickle cell disease for several reasons. Firstly, patients with sickle cell disease have higher IgE levels than the general population. Secondly, the mechanism of activation of molecular adhesion between endothelial and blood cells are similar between both sickle cell disease and atopic disease. Thirdly, the cytokines produced from platelet activation are the same cytokines that stimulate allergic inflammation in atopic diseases and promote adherence of sickle cells and endothelium in sickle cell disease. Lastly, sickle cell disease was reported to be associated with other atopic diseases.
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Smirnova, Galina I. "CURRENT CONCEPTS OF ATOPIC DERMATITIS IN CHILDREN: PROBLEMS AND PROSPECTS." Russian Pediatric Journal 20, no. 2 (April 30, 2019): 99–107. http://dx.doi.org/10.18821/1560-9561-2017-20-2-99-107.
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There are presented modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, apremilast, dupilumab, lebrikizumab, tralokinumab, tezepelumab. There is especially presented in details external therapy of atopic skin lesions in children with the use of means of modern dermatological cosmetics.
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Smirnova, G. I. "CURRENT CONCEPTS OF ATOPIC DERMATITIS IN CHILDREN: PROBLEMS AND PROSPECTS." Russian Journal of Allergy 14, no. 4-5 (December 15, 2017): 30–39. http://dx.doi.org/10.36691/rja292.
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Modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disturbances of the intestinal microbiome, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin are presented. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, dupilumab, apremilast et al. External therapy of atopic skin lesions in AD children with modern dermatological cosmetics is presented.
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Kay, A. B., S. Ying, V. Varney, M. Gaga, S. R. Durham, R. Moqbel, A. J. Wardlaw, and Q. Hamid. "Messenger RNA expression of the cytokine gene cluster, interleukin 3 (IL-3), IL-4, IL-5, and granulocyte/macrophage colony-stimulating factor, in allergen-induced late-phase cutaneous reactions in atopic subjects." Journal of Experimental Medicine 173, no. 3 (March 1, 1991): 775–78. http://dx.doi.org/10.1084/jem.173.3.775.
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Cryostat sections from skin biopsies from 24-h allergen-induced late-phase cutaneous reactions (LPR) in 14 human atopic subjects were hybridized with 35S-labeled RNA probes for a number of cytokines. mRNA was detected for interleukin 3 (IL-3) (8/14), IL-4 (10/14), IL-5 (11/14), and granulocyte/macrophage colony-stimulating factor (GM-CSF) (13/14). Only 5 of 14 gave hybridization signals for IL-2, and 0 of 14 for interferon gamma. Biopsies from diluent controls gave only occasional weak signals. These results suggest that cells infiltrating the site of the 24-h LPR transcribe mRNA for the IL-3, IL-4, IL-5, and GM-CSF gene cluster and support the hypothesis that atopy is associated with preferential activation of cells having a similar cytokine profile to the murine T helper type 2 subset.
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Teixeira, Renata, Gerson dos Santos Leite, Renata Gorjao, Patricia Palmeira, Cesar Santos, Raquel Zambonatto, Heloisa de Oliveira, Adriana Levada, Iara Fiks, and Celso Carvalho. "Immune and Inflammatory Response in Atopic Elite Endurance Athletes." International Journal of Sports Medicine 39, no. 09 (June 25, 2018): 720–25. http://dx.doi.org/10.1055/a-0633-9001.
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AbstractThe present study aimed to compare the immune and inflammatory responses between atopic (n=20) and non-atopic (n=39) elite endurance athletes. Fifty-nine elite runners and triathletes were assessed for the following measurements: Th1, Th2 and lymphocyte phenotyping and plasma levels of cortisol, chemokines, inflammatory cytokines and specific immunoglobulin E (IgE). Levels of salivary IgA, allergic symptoms and training data were also evaluated. No difference was observed in baseline lymphocyte levels. However, the Th1 lymphocytes of atopic athletes presented a lower response after activation. In contrast to this result, levels of salivary IgA and CXCL9 chemokine were higher in the atopic athletes. It was observed that the volume of training per week was linearly associated with Th1 levels, allergic symptoms and IgE levels. In addition, linear multiple regression analysis demonstrated that the volume of training was the only factor associated with allergic symptoms in atopic athletes (r=0.53; p=0.04). These results suggest that compared to non-atopic athletes, atopic athletes present a reduced Th1 response and higher levels of salivary IgA. Training volume is associated with the immune response and allergic symptoms, which suggests that they may play a role in the atopy in elite endurance athletes.
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Young, Sarah L., Mary A. Simon, Margaret A. Baird, Gerald W. Tannock, Rodrigo Bibiloni, Kate Spencely, Juliette M. Lane, et al. "Bifidobacterial Species Differentially Affect Expression of Cell Surface Markers and Cytokines of Dendritic Cells Harvested from Cord Blood." Clinical Diagnostic Laboratory Immunology 11, no. 4 (July 2004): 686–90. http://dx.doi.org/10.1128/cdli.11.4.686-690.2004.
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ABSTRACT The gut microbiota may be important in the postnatal development of the immune system and hence may influence the prevalence of atopic diseases. Bifidobacteria are the most numerous bacteria in the guts of infants, and the presence or absence of certain species could be important in determining the geographic incidence of atopic diseases. We compared the fecal populations of bifidobacteria from children aged 25 to 35 days in Ghana (which has a low prevalence of atopy), New Zealand, and the United Kingdom (high-prevalence countries). Natal origin influenced the detection of bifidobacterial species in that fecal samples from Ghana almost all contained Bifidobacterium infantis whereas those of the other children did not. Choosing species on the basis of our bacteriological results, we tested bifidobacterial preparations for their effects on cell surface markers and cytokine production by dendritic cells harvested from cord blood. Species-specific effects on the expression of the dendritic-cell activation marker CD83 and the production of interleukin-10 (IL-10) were observed. Whereas CD83 expression was increased and IL-10 production was induced by Bifidobacterium bifidum, Bifidobacterium longum, and Bifidobacterium pseudocatenulatum, B. infantis failed to produce these effects. We concluded that B. infantis does not trigger the activation of dendritic cells to the degree necessary to initiate an immune response but that B. bifidum, B. longum, and B. pseudocatenulatum induce a Th2-driven immune response. A hypothesis is presented to link our observations to the prevalence of atopic diseases in different countries.
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Elisyutina, O. G., M. N. Boldyreva, O. Yu Rebrova, and E. S. Fedenko. "AD endotypes evaluation with molecular-genetic analysis of local immune response." Russian Journal of Allergy 15, no. 6 (December 15, 2018): 33–44. http://dx.doi.org/10.36691/rja100.
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The basis for the development of atopic dermatitis (AD) is genetic predisposition, hypersensitivity to allergens, Th1/Th2 disbalance, increased degranulation of mast cells and antigen-presenting activity of Langerhans cells, as well as epidermal barrier dysfunction. Recently, genotypes, phenotypes and endotypes of AD, and biomarkers, which can be used to assess the effectiveness of therapy and to develop personalized approaches to the diagnosis, treatment and prognosis of the disease, have been actively studied. The aim of this study was to determine the endotypes of atopic dermatitis on the basis of molecular genetic study of cytokine gene expression in the skin of AD patients. Materials and methods. The study was performed as a «case-control», 90 AD patients and 30 healthy individuals without signs of atopy were included. The material for evaluation of cytokine gene expression was skin biopsy samples taken by punch biopsy. The level of gene expression was determined by real-time PCR with preliminary reverse transcription of mRNA of the corresponding genes («DNA-Technology», Moscow). The transcript levels of ILB, IL2, IL2r, IL4, IL5, IL6, IL7, IL8, IL10, IL12A, IL12B, IL15, IL17A, IL18, IL23, IL28, IL29, IFNy, TNF, TGFß, FOXP3 genes were studied. Results. Based on the molecular genetic study of the local immune response the following endotypes of AD were determined: endotype with predominance of Th1-type immune response (3% of patients); endotype with predominance of Th2-type immune response (3% of patients); mixed endotype with increased expression of IL2 (20% of patients); mixed endotype with reduced expression of IL10 (64% of patients); mixed endotype with increased expression of TGFß (9% of patients). Clinically significant biomarkers of inflammation in atopic dermatitis - decreased mRNA level of IL1ß gene expression and increased mRNA level of IL2R, IL4, IL5, IL6, IL8, IL10, IL12ß, IL23, IL29, IFNy and TGFß genes expression were determined in the skin of AD patients compared to healthy individuals. Conclusion. The use of molecular genetic method for evaluation of local immune response on the basis of cytokines gene expression measurement in the skin allows to identify the most significant biomarkers characterizing different endotypes of AD, and to determine the type of immune response in the individual patient.
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Zhang, Guicheng, Catherine M. Hayden, Jack Goldblatt, Patrick Holt, and Peter N. Le Souëf. "Th2 Cytokine Levels Distort the Association of IL-10 and IFN-γ with Allergic Phenotypes." ISRN Allergy 2011 (December 28, 2011): 1–6. http://dx.doi.org/10.5402/2011/405813.
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The expression of allergic phenotypes involves complex inter-relationships among several Th2 and Th1 cytokines as well as the regulator cytokine interleukin (IL)-10. These direct or indirect interrelationships may distort the true associations of cytokine responses with these phenotypes. In this study, we aimed to clarify the effects of the regulatory cytokine IL-10 and Th1 cytokine interferon-gamma (IFN-γ) on allergic phenotypes after adjusting for the correlations with Th2 cytokines. After adjusting for Th2 cytokines, IL-10 and IFN-γ were protective against atopy. Adjusted levels of IL-10 and IFN-γ stimulated with house-dust mite (HDM) were significantly lower in atopics than non-atopics, for IL-10 adjusting for IL-5 (P=0.002), IL-13 (P=0.012), IL-9 (P=0.016), and IL-4 (P=0.043), and for IFN-γ adjusting for IL-5 (P=0.005), IL-13 (P=0.005), and IL-9 (P=0.037). IL-10 and IFN-γ levels stimulated with phytohaemagglutinin (PHA) and staphylococcal enterotoxin B (SEB) exhibited a similar pattern. The adjusted levels of IL-10 and IFN-γ stimulated with HDM, PHA or SEB were all significantly negatively correlated with total serum IgE, except for IFN-γ stimulated with SEB. Levels of Th2 cytokines distort the associations of IL-10 and IFN-γ with allergic phenotypes. Removing the covariance with Th2 cytokines, both IL-10 and IFN-γ were protective against atopy.
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Pinto, Leonardo Araujo, Renato Tetelbom Stein, and José Dirceu Ribeiro. "Genetic associations with asthma and virus-induced wheezing: a systematic review." Jornal Brasileiro de Pneumologia 35, no. 12 (December 2009): 1220–26. http://dx.doi.org/10.1590/s1806-37132009001200010.
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Various wheezing phenotypes can be identified based on differences in natural histories, risk factors and responses to treatment. In epidemiologic studies, atopic asthma or virus-induced wheezing can be discriminated by the presence or the absence of sensitization to allergens. Children with asthma have been shown to present lower levels of lung function. Patients with viral respiratory infections evolve from normal lung function to enhanced airway reactivity. The objective of this study was to identify genes and polymorphisms associated with different wheezing phenotypes. Using data obtained from the Genetic Association Database, we systematically reviewed studies on genes and polymorphisms that have been associated with virus-induced wheezing or atopic asthma. The research was carried out in February of 2009. Genes associated with the studied outcomes in more than three studies were included in the analysis. We found that different genes and loci have been associated with virus-induced wheezing or atopic asthma. Virus-induced wheezing has frequently been associated with IL-8 polymorphisms, whereas atopic asthma and atopy have frequently been associated with Th2 cytokine gene (CD14 and IL-13) polymorphisms on chromosome 5. This review provides evidence that different wheezing disorders in childhood can be differently affected by genetic variations, considering their role on airway inflammation and atopy. Future studies of genetic associations should consider the different wheezing phenotypes in infancy. In addition, stratified analyses for atopy can be useful for elucidating the mechanisms of the disease.
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Milner, Joshua D. "Primary Atopic Disorders." Annual Review of Immunology 38, no. 1 (April 26, 2020): 785–808. http://dx.doi.org/10.1146/annurev-immunol-042718-041553.
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Primary atopic disorders describes a series of monogenic diseases that have allergy- or atopic effector–related symptoms as a substantial feature. The underlying pathogenic genetic lesions help illustrate fundamental pathways in atopy, opening up diagnostic and therapeutic options for further study in those patients, but ultimately for common allergic diseases as well. Key pathways affected in these disorders include T cell receptor and B cell receptor signaling, cytokine signaling, skin barrier function, and mast cell function, as well as pathways that have not yet been elucidated. While comorbidities such as classically syndromic presentation or immune deficiency are often present, in some cases allergy alone is the presenting symptom, suggesting that commonly encountered allergic diseases exist on a spectrum of monogenic and complex genetic etiologies that are impacted by environmental risk factors.
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Marques, Vanessa Stuart, Jessica Ragazzi Celesso, and Adriane Pimenta da Costa Val Bicalho. "Evaluation of quality of life in dogs with atopic dermatitis and their owners after lokivetmab therapy." Research, Society and Development 10, no. 11 (September 5, 2021): e392101119775. http://dx.doi.org/10.33448/rsd-v10i11.19775.
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Canine atopic dermatitis is an inflammatory and pruritic skin disease, with clinical characteristics associated with IgE antibodies, most commonly directed against environmental allergens which impact the quality of life in affected animals and their owners. Treatment is multifaceted and must be adapted to each patient individually. Currently, a medication based on caninized monoclonal antibody (mAb), called lokivetmab, has shown promise for controlling the signs of the disease, as it neutralizes interleukin IL-31, a cytokine that plays an important role in the pathogenesis of atopy. The impact of dermatological diseases in the life of the dog and its owner has only been studied in recent years through validated questionnaires. This additional measurement tool is important for evaluating the therapeutic success of interventions in atopic dermatitis, as clinical improvement may not correlate with an increased quality of life. This study aimed to evaluate the quality of life in dogs with atopic dermatitis and their owners after lokivetmab therapy. Ten atopic dogs treated at the dermatology service of the Veterinary Hospital of the Veterinary School from UFMG were selected. Quality of life was assessed using a validated questionnaire, before and after lokivetmab therapy. It concludes that treatment with lokivetmab significantly improved the quality of life of dogs with atopic dermatitis and their owners.
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Briot, Anaïs, Céline Deraison, Matthieu Lacroix, Chrystelle Bonnart, Aurélie Robin, Céline Besson, Pierre Dubus, and Alain Hovnanian. "Kallikrein 5 induces atopic dermatitis–like lesions through PAR2-mediated thymic stromal lymphopoietin expression in Netherton syndrome." Journal of Experimental Medicine 206, no. 5 (May 4, 2009): 1135–47. http://dx.doi.org/10.1084/jem.20082242.
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Netherton syndrome (NS) is a severe genetic skin disease with constant atopic manifestations that is caused by mutations in the serine protease inhibitor Kazal-type 5 (SPINK5) gene, which encodes the protease inhibitor lymphoepithelial Kazal-type–related inhibitor (LEKTI). Lack of LEKTI causes stratum corneum detachment secondary to epidermal proteases hyperactivity. This skin barrier defect favors allergen absorption and is generally regarded as the underlying cause for atopy in NS. We show for the first time that the pro-Th2 cytokine thymic stromal lymphopoietin (TSLP), the thymus and activation-regulated chemokine, and the macrophage-derived chemokine are overexpressed in LEKTI-deficient epidermis. This is part of an original biological cascade in which unregulated kallikrein (KLK) 5 directly activates proteinase-activated receptor 2 and induces nuclear factor κB–mediated overexpression of TSLP, intercellular adhesion molecule 1, tumor necrosis factor α, and IL8. This proinflammatory and proallergic pathway is independent of the primary epithelial failure and is activated under basal conditions in NS keratinocytes. This cell-autonomous process is already established in the epidermis of Spink5−/− embryos, and the resulting proinflammatory microenvironment leads to eosinophilic and mast cell infiltration in a skin graft model in nude mice. Collectively, these data establish that uncontrolled KLK5 activity in NS epidermis can trigger atopic dermatitis (AD)–like lesions, independently of the environment and the adaptive immune system. They illustrate the crucial role of protease signaling in skin inflammation and point to new therapeutic targets for NS as well as candidate genes for AD and atopy.
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Ogorodova, L. M., O. S. Fyodorova, M. B. Freidin, M. B. Vasil’yeva, N. A. Cherevko, A. E. Sazonov, I. V. Petrova, et al. "Characteristics of epidemiological and molecular relationships between allergic diseases and helminth disorders in Opisthorchis endemic region." Bulletin of Siberian Medicine 7, no. 4 (December 30, 2008): 37–44. http://dx.doi.org/10.20538/1682-0363-2008-4-37-44.
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To elucidate the molecular mechanisms of O. felineus impact into phenotypic variability of allergic diseases in the opisthorchis endemic region, we studied 104 patients with opisthorchosis, 92 patients with atopic bronchial asthma, 52 patients with a combination of both diseases, and 120 healthy persons. Standard clinical, immunological, and genetic methods were used. An association of opisthorchis invasion with the improvement of lung function signs and bronchial hyperreactivity was found. It was established, that IL-4-dependent mechanisms of atopy were suppressed by O. felineus antigens, in particular due to hyperproduction of IL-10 and transforming growth factor-beta. However, IL-5-dependant mechanisms were supported. A phenomenology of the cytokine gene differential expression was established, disclosing the molecular basis of the immune system function in diseases with polar immune response in the helminth endemic region.
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Esenboga, Saliha, Pınar Gur Cetinkaya, Neriman Sahiner, Esra Birben, Ozge Soyer, Bulent Enis Sekerel, and Umit Murat Sahiner. "Infantile atopic dermatitis: Serum vitamin D, zinc and TARC levels and their relationship with disease phenotype and severity." Allergologia et Immunopathologia 49, no. 3 (May 1, 2021): 162–68. http://dx.doi.org/10.15586/aei.v49i3.191.
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Background: Several markers that influence the clinical course of atopic dermatitis (AD) have been investigated so far. Thymus and activation regulated chemokine (TARC) – a Th2-related cytokine – increase in various atopic diseases. It has been shown that vitamin D affects Treg cells and immune responses. Zinc as an essential trace element for cell–cell interactions, cellular differentiation, and proliferation. However, the effect of these markers on infantile AD and disease severity are mostly unknown.Objective: The aim of this study was to investigate the relationship between TARC, vitamin D, zinc levels, and the disease severity in infants with AD.Method: AD patients (n = 160) with age and sex that matched healthy controls (n = 79) were included in the study. The diagnosis of AD was made based on the Hanifin–Rajka criteria. The objective SCORAD index was used for the assessment of disease severity.Results: A total of 160 patients (male 71.9%) with AD were included in the study. The median age of onset of symptoms was 2 (1.0–3.5) months. The lesions initially started on face 76.9%, neck 6.9%, extremities 7.5%, and body 8.8%. Nearly 40% of the patients were found to be atopic. Food allergy was found in 39.4%. The median of objective SCORAD index was 27.5 (17.5–40) in the study group. The TARC levels of AD patients were higher than control group [1803 pg/ml (1006– 3123) vs 709 pg/ml (504–1147), p < 0.001] There was a significant correlation between objective SCORAD scores and TARC values in subjects with AD (r = 0.363, p < 0.001). As the severity of AD increased, vitamin D levels decreased (p for trend 0.015) and TARC values increased (p for trend < 0.001). Serum zinc levels did not change with the severity of the disease. The presence of atopy did not have an influence on serum TARC, zinc, and vitamin D levels.Conclusion: In infants with AD, disease severity is positively related with TARC levels; and inversely proportional to vitamin D levels. TARC levels differ between patients and healthy controls. The presence of atopy has not been shown to affect these markers.
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Chen, Yi-Ling, Danuta Gutowska-Owsiak, Clare S. Hardman, Melanie Westmoreland, Teena MacKenzie, Liliana Cifuentes, Dominic Waithe, et al. "Proof-of-concept clinical trial of etokimab shows a key role for IL-33 in atopic dermatitis pathogenesis." Science Translational Medicine 11, no. 515 (October 23, 2019): eaax2945. http://dx.doi.org/10.1126/scitranslmed.aax2945.
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Targeted inhibition of cytokine pathways provides opportunities to understand fundamental biology in vivo in humans. The IL-33 pathway has been implicated in the pathogenesis of atopy through genetic and functional associations. We investigated the role of IL-33 inhibition in a first-in-class phase 2a study of etokimab (ANB020), an IgG1 anti–IL-33 monoclonal antibody, in patients with atopic dermatitis (AD). Twelve adult patients with moderate to severe AD received a single systemic administration of etokimab. Rapid and sustained clinical benefit was observed, with 83% achieving Eczema Area and Severity Index 50 (EASI50), and 33% EASI75, with reduction in peripheral eosinophils at day 29 after administration. We noted significant reduction in skin neutrophil infiltration after etokimab compared with placebo upon skin challenge with house dust mite, reactivity to which has been implicated in the pathogenesis of AD. We showed that etokimab also inhibited neutrophil migration to skin interstitial fluid in vitro. Besides direct effects on neutrophil migration, etokimab revealed additional unexpected CXCR1-dependent effects on IL-8–induced neutrophil migration. These human in vivo findings confirm an IL-33 upstream role in modulating skin inflammatory cascades and define the therapeutic potential for IL-33 inhibition in human diseases, including AD.
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Renke, Joanna, Eliza Wasilewska, Sabina Kędzierska-Mieszkowska, Katarzyna Zorena, Sylwia Barańska, Tomasz Wenta, Anna Liberek, et al. "Tumor Suppressors—HTRA Proteases and Interleukin-12—in Pediatric Asthma and Allergic Rhinitis Patients." Medicina 56, no. 6 (June 17, 2020): 298. http://dx.doi.org/10.3390/medicina56060298.
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Background and objective: Allergy belongs to a group of mast cell-related disorders and is one of the most common diseases of childhood. It was shown that asthma and allergic rhinitis diminish the risk of various cancers, including colon cancer and acute lymphoblastic leukemia. On the other hand, asthma augments the risk of lung cancer and an increased risk of breast cancer in patients with allergy has been observed. Thus, the relation between allergy and cancer is not straightforward and furthermore, its biological mechanism is unknown. The HTRA (high temperature requirement A) proteases promote apoptosis, may function as tumor suppressors and HTRA1 is known to be released by mast cells. Interleukin-12 (Il-12) is an important cytokine that induces antitumor immune responses and is produced mainly by dendritic cells that co-localize with mast cells in superficial organs. Material and methods: In the present study we have assessed with ELISA plasma levels of the HTRA proteins, Il-12, and of the anti-HTRA autoantibodies in children with allergy (40) and in age matched controls (39). Children are a special population, since they usually do not have comorbidities and take not many drugs the processes we want to observe are not influenced by many other factors. Results: We have found a significant increase of HTRA1, 2 and 3, and of the Il-12 levels in the children with atopy (asthma and allergic rhinitis) compared to controls. Conclusion: Our results suggest that the HTRA1–3 and Il-12 levels might be useful in analyzing the pro- and antioncogenic potential in young atopic patients.
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McMenamin, C., and P. G. Holt. "The natural immune response to inhaled soluble protein antigens involves major histocompatibility complex (MHC) class I-restricted CD8+ T cell-mediated but MHC class II-restricted CD4+ T cell-dependent immune deviation resulting in selective suppression of immunoglobulin E production." Journal of Experimental Medicine 178, no. 3 (September 1, 1993): 889–99. http://dx.doi.org/10.1084/jem.178.3.889.
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The immunological basis for atopy is currently ascribed to an inherent bias in the CD4+ T cell response to nonreplicating antigens presented at mucosal surfaces, resulting in dominance of the T helper 2 (Th2) interleukin 4 (IL-4)-producing phenotype, which favors IgE production. In contrast, the "normal" response to such antigens involves a predominance of interferon gamma (IFN-gamma)-producing Th1 clones. This difference has been suggested to be the result of active selection in atopics for Th2 (and hence against Th1) clones at the time of initial antigen presentation. In the study below, we demonstrate that the natural immune response to inhaled protein antigens, particularly in animals expressing the low immunoglobulin E (IgE) responder phenotype, includes a major histocompatibility complex (MHC) class I-restricted CD8+ T cell component, the appearance of which is associated with active suppression of IgE antibody production. Thus, continued exposure of rats to aerosolized ovalbumin (OVA) antigen elicits a transient IgE response, that is terminated by the onset of a state of apparent "tolerance" to further challenge, and this tolerant state is transferable to naive animals with CD8+ T cells. Kinetic studies on in vitro T cell reactivity in these aerosol-exposed rats demonstrated biphasic CD4+ Th2 responses which terminated, together with IgE antibody production, and coincident with the appearance of MHC class I-restricted OVA-specific IFN-gamma-producing CD8+ T cells. However, the latter were not autonomous in vitro and required a source of exogenous IL-2 for initial activation, which in CD(8+)-enriched splenocyte cultures could be provided by small numbers of contaminating OVA-specific CD4+ T cells. This represents the first formal evidence for the induction of an MHC class I-restricted T cell response to natural mucosal exposure to an inert protein antigen, and is consistent with a growing literature demonstrating sensitization of MHC class I-restricted CD8+ T cells by deliberate immunization with soluble proteins. We suggest that crossregulation of MHC class II-restricted CD4+ T cells via cytokine signals generated in parallel CD8+ T cell responses represents a covert and potentially important selection pressure that can shape the nature of host responses to nonreplicating antigens presented at mucosal surfaces.
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Utama, Budi, Heri Wibowo, and Niken Lestari Poerbonegoro. "Efek vitamin D terhadap kadar IL-10, IFN-γ, dan histamin pada kultur PBMC pasien rinitis alergi." Oto Rhino Laryngologica Indonesiana 47, no. 2 (January 7, 2018): 132. http://dx.doi.org/10.32637/orli.v47i2.222.
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Latar belakang: Rinitis alergi (RA) adalah penyakit inflamasi pada hidung, yang disebabkan oleh reaksi alergi pada pasien atopi. Tungau debu rumah merupakan aeroalergen yang tersering memicu reaksi alergi. Pada tahun 1988, reseptor vitamin D berhasil dilakukan klon. Reseptor vitamin D berlokasi di beberapa jaringan dan sel tubuh manusia, termasuk di sel-sel darah tepi berinti tunggal (peripheral blood mononuclear cells/PMBC). Tujuan: Mengidentifikasi pengaruh pemberian vitamin D pada sel-sel darah tepi berinti tunggal penderita rinitis alergi terhadap sel Th1, Th2, dan T Regulator, dengan cara melihat sekresi IFN-γ, IL-10, dan histamin. Metode: Sampel berupa darah segar (whole blood) penderita rinitis alergi yang telah dilakukan prick test, diolah dengan metode Ficoll untuk mengisolasi sel berinti tunggal. Kultur sel limfosit sebelum perlakuan dibagi menjadi kelompok yang diberi pendedahan dengan 1,25(OH)2D3 100 nM dan tanpa pendedahan, waktu inkubasi 7 hari, dengan penambahan phytohaemaglutinin dan alergen tungau pada hari ke-4. Kultur sel-sel darah tepi berinti tunggal dari pasien RA setelah perlakuan, selanjutnya pada hari ke-7 supernatannya diambil dan dibagi untuk diukur kadar sitokin IFN-γ, IL-10, dan histamin secara ELISA. Dilakukan uji secara statistik untuk melihat pola dari tiap parameter. Hasil: Pemberian alergen tungau tanpa vitamin D menyebabkan meningkatnya kadar histamin serta menurunkan kadar IL-10 dan IFN-γ. Pemberian vitamin D pada kultur sel darah tepi berinti tunggal yang telah diberi alergen tungau, dapat meningkatkan kadar IL-10 dan menurunkan kadar IFN-γ, serta histamin. Kesimpulan: Menurunnya kadar histamin dan IFN-γ terhadap stimulasi alergen tungau pada pasien rinitis alergi yang diberi vitamin D cenderung berhubungan dengan meningkatnya kadar IL-10. Kata kunci: Sel mast, rinitis alergi, tungau debu rumah, vitamin D ABSTRACT Background: Allergic rhinitis is an inflammatory disease of the nose, caused by an allergic reaction in atopic patients. House dust mites are the most common aeroalergen. In 1988, vitamin D receptor had been cloned successfully. Vitamin D receptors are located in various tissues and human body cells, including peripheral blood mononuclear cells (PBMCs). Purpose: To identify the effect of vitamin D on peripheral blood mononuclear cells culture of allergic rhinitis patients towards Th1, Th2, and T Regulator cell, by identifying IL-10, IFN-γ, and histamine secretion levels. Method: The sample were obtained from fresh blood (whole blood) of allergic rhinitis patients who had been prick tested, and isolated by Ficoll method. Pre-treated lymphocyte culture divided into groups treated with and without 1,25(OH)2D3 100 nM, and incubated for 7 days, with addition of phytohaemaglutinin and allergen mites on day 4. Cultures of PBMC cells after treatment were harvested on day 7, then the supernatant was dialyzed to measure the levels of IFN-γ IL-10 and histamine cytokines. Statistical test was performed to identify patterns of each parameter. Results: Treatment of allergen mites without vitamin D could increase levels of histamine and lower levels of IL-10 and IFN-γ. Provision of vitamin D in PBMC cell culture that had been given allergen mites could increase levels of IL-10 and decreased levels of IFN-γ and histamine. Conclusion: Lower levels of histamine and IFN-γ against allergen mite stimulation of allergic rhinitis patients who were given vitamin D tend to be associated with increased IL-10 levels. Keywords: Mast cell, allergic rhinitis, house dust mite, vitamin D
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Maura, Damien, Nazik Elmekki, and C. Alex Goddard. "The ammonia oxidizing bacterium Nitrosomonas eutropha blocks T helper 2 cell polarization via the anti-inflammatory cytokine IL-10." Scientific Reports 11, no. 1 (July 8, 2021). http://dx.doi.org/10.1038/s41598-021-93299-1.
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AbstractThe prevalence of atopic diseases has been steadily increasing since the mid twentieth century, a rise that has been linked to modern hygienic lifestyles that limit exposure to microbes and immune system maturation. Overactive type 2 CD4+ helper T (Th2) cells are known to be closely associated with atopy and represent a key target for treatment. In this study, we present an initial characterization of ammonia oxidizing bacteria (AOB) Nitrosomonas eutropha D23, an environmental microbe that is not associated with human pathology, and show AOB effectively suppress the polarization of Th2 cells and production of Th2-associated cytokines (IL-5, IL-13, and IL-4) by human peripheral blood mononuclear cells (PBMC). We show that AOB inhibit Th2 cell polarization not through Th1-mediated suppression, but rather through mechanisms involving the anti-inflammatory cytokine IL-10 and the potential inhibition of dendritic cells, as evidenced by a reduction in Major Histocompatibility Complex Class II (MHC II) and CD86 expression following AOB treatment. This is the first report of immunomodulatory properties of AOB, and provides initial support for the development of AOB as a potential therapeutic for atopic diseases.
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Gamez, Cristina, Jessica Metcalfe, Susan L. Prescott, and Debra J. Palmer. "Lower Cord Blood IL-17 and IL-25, but Not Other Epithelial Cell-Derived Cytokines Are Associated with Atopic Dermatitis in Infancy." International Archives of Allergy and Immunology, January 7, 2021, 1–5. http://dx.doi.org/10.1159/000512919.
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<b><i>Background:</i></b> There is a growing need for early biomarkers that may predict the development of atopic dermatitis (AD). As alterations in skin barrier may be a primary event in disease pathogenesis, epithelial cell (EC) cytokines expression patterns may be a potential biomarker in early life to target allergy preventive strategies towards “at-risk” infants. <b><i>Objectives:</i></b> The aim of this longitudinal investigation was to examine from birth over the course of infancy levels of the EC cytokines: thymic stromal lymphopoietin (TSLP), interleukin (IL)-33, IL-25, and IL-17 in infants at high-risk of AD due to maternal atopy. <b><i>Method:</i></b> We collected (<i>n</i> = 31) cord blood samples from atopic mothers and followed up their infants at 4–6 and 12 months of age for collection of peripheral venous blood samples and diagnosis of AD. TSLP concentration was measured by ELISA after acetone precipitation of the samples. IL-33, IL-25, and IL-17 levels were measured by Luminex. <b><i>Results:</i></b> Seven infants who developed AD had lower levels of IL-25 and IL-17 at birth compared to the 24 infants who did not develop AD by 12 months of age. <b><i>Conclusions:</i></b> Lower cord blood levels of IL-17 and IL-25, but not other EC cytokines, were associated with the onset of AD during infancy. Our results highlight that the in-utero period appears critical, and potential maternal influences on cord blood EC-derived cytokine concentrations requires further exploration.
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Madeira, Leticia Nabuco de Oliveira, Maria Alice Neves Bordallo, Marcos Antonio Borges, Agnaldo José Lopes, Isabel Rey Madeira, and Fábio Chigres Kuschnir. "RELATIONS BETWEEN ASTHMA AND OBESITY: AN ANALYSIS OF MULTIPLE FACTORS." Revista Paulista de Pediatria 39 (2021). http://dx.doi.org/10.1590/1984-0462/2021/39/2019405.
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ABSTRACT Objective: Asthma and obesity are prevalent and interrelated diseases. In the pediatric population, the effect of systemic inflammation associated to obesity, leading to inflammation of the airways, is currently controversial. Our aim was to compare inflammatory, clinical and spirometric patterns between children with asthma and obesity and those within the normal weight status range. Methods: A total of 79 boys and girls from 6 to 10 years old were selected and divided into four groups: obese asthmatics, non-obese asthmatics, obese non-asthmatics, and non-obese non-asthmatics. In addition to collecting clinical and anthropometric data, all children underwent spirometry and skin prick tests for inhalant allergens. Blood samples for measurement of cytokines and adipokines were also collected. Results: Obese asthmatics had significantly worse control of asthma than non-obese asthmatics (OR 4.9; 95%CI 1.1‒22.1), regardless of sex, physical activity and atopy. No differences in spirometry, Th1 and Th2 cytokines and adipokines levels were observed among the four groups. The prick tests were positive in 81.8 and 80% of non-obese asthmatics and obese asthmatics, respectively. Conclusions: The degree of control of asthma was significantly lower in the obese group, regardless of the findings of no differences in spirometry. Extra-pulmonary factors could be responsible for this symptomatic profile. High positivity of skin test in both groups, which is considered a good marker of atopy, shows a preponderant atopic component in the genesis of asthma, both in children with obesity and in those within the normal weight status.
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Pandaleke, Thigita A., and Herry E. J. Pandaleke. "ETIOPATOGENESIS DERMATITIS ATOPI." JURNAL BIOMEDIK (JBM) 6, no. 2 (September 11, 2014). http://dx.doi.org/10.35790/jbm.6.2.2014.5547.
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Abstract: Atopic dermatitis is a chronically relapsing skin disease that occurs most commonly during early infancy and childhood. It is a major public health problem worldwide with a prevalence in children 10-20% and 1-3% in adults. However, its main etiology is uncertain. There are some initiating factors that play important roles in the occurence and progress of this dermatitis atopic, such as: decreased skin barrier function, dysfunction of the immune system, genetic factor, enviromental factors, and infections, involving the immune system in the blood as well as in the skin, cytokines, and peptides. Keywords: atopic dermatitis, initiating factors Abstrak: Dermatitis atopi adalah penyakit kulit kronik kambuhan yang paling sering terjadi pada bayi dan anak-anak. Penyakit ini merupakan masalah kesehatan utama di seluruh dunia, dengan prevalensi 10-20% pada anak dan 1-3% pada dewasa. Penyebab pasti dermatitis atopi belum diketahui. Terdapat beberapa faktor pencetus yang diduga turut berperan dalam terjadinya dan perlangsungan dermatitis atopi, antara lain: interaksi antara penurunan fungsi sawar kulit, disfungsi sistem imun, faktor genetik, faktor lingkungan, dan agen infeksi, dengan melibatkan berbagai sistem imun baik di dalam darah maupun pada kulit, sitokin, dan peptida. Kata kunci: dermatitis atopi, faktor pencetus
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Wohlmann, Andreas, Katrin Sebastian, Andreas Borowski, Sebastian Krause, and Karlheinz Friedrich. "Signal transduction by the atopy-associated human thymic stromal lymphopoietin (TSLP) receptor depends on Janus kinase function." Biological Chemistry 391, no. 2/3 (January 1, 2010). http://dx.doi.org/10.1515/bc.2010.029.
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Abstract Thymic stromal lymphopoietin (TSLP) is an interleukin-(IL)-7-like cytokine with emerging pathological importance for the development of atopic diseases such as allergic asthma bronchiale. The TSLP receptor (TSLPR), a heterodimeric type I cytokine receptor, shares the IL-7R α-subunit with the IL-7 receptor system. The specific TSLPR α-chain shows similarities with the γc receptor chain, but has some unusual features within the receptor family in both its ligand-binding and cytoplasmic domain. The murine TSLPR signals via the signal transducers and activators of transcription STAT5 and STAT3, but is unique among cytokine receptors in that it activates STATs without the involvement of Janus (JAK) tyrosine kinases, but instead utilizes the Src type kinase Tec. Here, we show by Western blotting and reporter gene experiments in combination with the application of a specific JAK inhibitor that the human TSLP receptor, in contrast, requires the function of JAK1 and JAK2 for STAT activation. Moreover, we demonstrate that the human TSLPR mediates gene regulation not only through STAT5 and STAT3 but has also the potential to mediate transcription via STAT1. Our work should help to understand more thoroughly how TSLP triggers inflammatory responses in the course of atopic diseases.