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Sökning: L773:1423 0097 OR L773:1018 2438

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1.
  • Abbasi-Dokht, T, et al. (författare)
  • Multistrain Probiotics Supplement Alleviates Asthma Symptoms via Increasing Treg Cells Population: A Randomized, Double-Blind, Placebo-Controlled Trial
  • 2023
  • Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 184:3, s. 291-301
  • Tidskriftsartikel (refereegranskat)abstract
    • <b><i>Introduction:</i></b> The favorable effects of probiotics have been demonstrated in allergic disorders. However, the underlying immunological mechanisms are poorly understood. In the present study, we investigated the improvement of clinical symptoms and immunological balance after receiving probiotics in patients with asthma. <b><i>Methods:</i></b> The present study was a randomized, double-blind, placebo-controlled trial in which 40 patients with asthma were enrolled. They were treated with probiotics or placebo: 1 capsule/day for 8 weeks. Pulmonary function test, percentage of CD4<sup>+</sup> CD25<sup>+</sup> FoxP3<sup>+</sup> Tregs, and gene expression of T-bet, GATA-3, RORγt, and Foxp3 in PBMCs were assessed at baseline and after treatment. <b><i>Results:</i></b> Our results showed a significant increase in the expression of FoxP3 and CD4<sup>+</sup> CD25<sup>+</sup> FoxP3<sup>+</sup> Tregs population, while RORγt and GATA3 expression were reduced. In addition, pulmonary function tests showed a significant improvement in forced expiratory volume and forced vital capacity after receiving probiotics. <b><i>Discussion/Conclusion:</i></b> Our findings demonstrate that 8-week treatment with probiotic supplementation can control T-helper 2-predominant and Th17 pro-inflammatory responses and improve forced vital and forced expiratory volume in asthmatic patients. It seems probiotics can be used besides common treatments for patients with asthma.
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2.
  • Accordini, Simone, et al. (författare)
  • The Cost of Persistent Asthma in Europe : An International Population-Based Study in Adults
  • 2013
  • Ingår i: International Archives of Allergy and Immunology. - : S. Karger AG. - 1018-2438 .- 1423-0097. ; 160:1, s. 93-101
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: This study is aimed at providing a real-world evaluation of the economic cost of persistent asthma among European adults according to the degree of disease control [as defined by the 2006 Global Initiative for Asthma (GINA) guidelines]. Methods: A prevalence-based cost-of-illness study was carried out on 462 patients aged 30-54 years with persistent asthma (according to the 2002 GINA definition), who were identified in general population samples from 11 European countries and examined in clinical settings in the European Community Respiratory Health Survey II between 1999 and 2002. The cost estimates were computed from the societal perspective following the bottom-up approach on the basis of rates, wages and prices in 2004 (obtained at the national level from official sources), and were then converted to the 2010 values. Results: The mean total cost per patient was EUR 1,583 and was largely driven by indirect costs (i.e. lost working days and days with limited, not work-related activities 62.5%). The expected total cost in the population aged 30-54 years of the 11 European countries was EUR 4.3 billion (EUR 19.3 billion when extended to the whole European population aged from 15 to 64 years). The mean total cost per patient ranged from EUR 509 (controlled asthma) to EUR 2,281 (uncontrolled disease). Chronic cough or phlegm and having a high BMI significantly increased the individual total cost. Conclusions: Among European adults, the cost of persistent asthma drastically increases as disease control decreases. Therefore, substantial cost savings could be obtained through the proper management of adult patients in Europe.
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3.
  • Aghamohammadi, A, et al. (författare)
  • Progression of selective IgA deficiency to common variable immunodeficiency
  • 2008
  • Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 147:2, s. 87-92
  • Tidskriftsartikel (refereegranskat)abstract
    • Selective IgA deficiency (IgAD) is the most common primary immunodeficiency in Caucasians. Although it is often asymptomatic, selected patients show an increased frequency of infections, allergies and autoimmune manifestations. Common variable immunodeficiency (CVID) is a primary antibody deficiency disease that shares many clinical features with IgAD. A common genetic basis for IgAD and CVID has been suggested based on their occurrence in members of the same family and the similarity of the underlying B cell defects. Progression from IgAD to CVID has also been reported in several cases. Here we present 4 patients with IgAD and autoimmune features who subsequently developed CVID. All symptomatic IgAD patients, especially those with associated IgG subclass deficiency or autoimmune features, should be monitored for evolution to CVID. Early diagnosis of this conversion and institution of immunoglobulin therapy is effective in preventing severe bacterial infections and pulmonary insufficiency.
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4.
  • Ahlstedt, S, et al. (författare)
  • Enhancement of the bronchial reactivity in immunized rats by neonatal treatment with capsaicin.
  • 1986
  • Ingår i: International archives of allergy and applied immunology. - : S. Karger AG. - 0020-5915 .- 1018-2438 .- 1423-0097. ; 80:3, s. 262-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Rats were injected with capsaicin at 1-2 days of age to abolish the content of substance P (SP) in nerve terminals. At 6 weeks of age the capsaicin-treated and control rats were sensitized daily for 1 or 2 subsequent weeks Monday through Friday with ovalbumin (OA). The OA was given without adjuvant as 300 ng subcutaneous (s.c.) injections in the neck region or as 1% aerosol for 30 min. The capsaicin-treated animals which were sensitized s.c. for 2 weeks reacted moderately with increased transpulmonary pressure (TPP) to airway challenge with OA, and strongly to intravenous (i.v.) challenge with OA or serotonin. The capsaicin-untreated animals, which were sensitized with OA, reacted weakly to the challenge. In the challenge. In the animals sensitized with aerosolized OA, slightly lower reactivity was seen compared with those sensitized s.c. Untreated and unsensitized control rats reacted only to serotonin challenge. No animal had any detectable serum or bronchial IgE antibodies. Aerosol-sensitized animals had IgG antibodies in both serum and bronchial lavage. Histologically, the animals treated with capsaicin in contrast to the untreated controls demonstrated a pronounced increase of lymphoid tissue around their bronchi. Their mast cell numbers were increased around vessels and in the pleura and their mucous cell numbers were increased in the epithelium of the bronchi and bronchioli. The sensitization did not add much to this histological picture.
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5.
  • Aniansson Zdolsek, Helena, 1961-, et al. (författare)
  • Expression of the T–cell markers CD3, CD4 and CD8 in healthy and atopic Children during the first 18 months of life
  • 1999
  • Ingår i: International Archives of Allergy and Immunology. - : S. Karger AG. - 1018-2438 .- 1423-0097. ; 119:1, s. 6-12
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: There is little information available about the development of T–cell immunity in healthy and atopic children. We have studied prospectively the mean fluorescence intensity of the T–cell receptor complex–associated CD3, CD4 and CD8 in relation to atopic family history (AFH) and the development of atopic disease.Methods: Children with a defined AFH (n = 172) were followed from birth to 18 months and the cumulative history of atopic disease was recorded. Blood samples were obtained at birth and at 18 months, and in a subgroup of 78 children also at 3, 6 and 12 months. Multicolour flow cytometry was used to analyse pan T–cells (CD3+CD45+CD14–), T–helper–(CD3+CD4+) and T–cytotoxic–(CD3+CD8+) cells.Results: At 18 months, 31 children were atopic and 118 non–atopic. Children who developed atopic disease had a higher CD4 expression (mean fluorescence intensity, MFI) on CD4+CD3+ lymphocytes at birth and at 3 months, particularly as compared with non–atopic children without AFH. Furthermore, the CD3 expression on CD3+CD45+CD14– lymphocytes increased more slowly with age in children with double atopic heredity, as compared with children with no or only one atopic family member.Conclusions: The higher expression of the CD4 receptor in early infancy in children who developed atopic disease compared with non–atopics suggests a delayed expression in T–helper cells. Children with a strong AFH had a slower increase in the expression of CD3, indicating a delayed T–cell maturation.
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6.
  • Ankerst, Jaro, et al. (författare)
  • Xolair Is Effective in Allergics with a Low Serum IgE Level.
  • 2010
  • Ingår i: International Archives of Allergy and Immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 152:1, s. 71-74
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Two atopic patients suffering from severe allergy difficult to handle by conventional medication were given Xolair despite an IgE level <30 kU/l. Methods: Increasing dosages were given and monitored by clinical evaluation and CD-sens to clinically relevant allergens. The patients' IgE antibody fractions were 11-14%. Results: Xolair dosages extrapolated from a recommended dose for IgE of 30-75 kU/l were adapted to the patients' IgE body pool but had very little effect. The double dose resulted in some clinical improvement and a decrease in CD-sens. However, not until the dose was doubled again did the patients become symptom free, although 1 patient needed some additional drugs but no oral steroids. CD-sens turned negative to 5 of the 7 tested allergens. Conclusions: Xolair is most useful also in atopics with an IgE level <30 kU/l. The dose must be adjusted to the size of the IgE antibody fraction adding all non-cross-reacting, clinically relevant specificities.
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7.
  • Anthoni, M, et al. (författare)
  • Smad3 regulates dermal cytokine and chemokine expression and specific antibody production in murine responses to a respiratory chemical sensitizer
  • 2010
  • Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 151:2, s. 155-167
  • Tidskriftsartikel (refereegranskat)abstract
    • <i>Background:</i> The cytokine transforming growth factor-β(TGF-β) has important regulatory roles in the immune system. To investigate the role of intact TGF-β signaling during the contact hypersensitivity (CHS) response to a respiratory allergen, we exposed Smad3–/– mice to topical trimellitic anhydride (TMA). <i>Methods:</i> CHS was induced by topical application of TMA. The swelling of the TMA-exposed ears was analyzed, and lymph node, ear tissue and skin biopsies were collected for RNA isolation, histology and histochemical analyses. Lymph node cell proliferation was measured and blood samples were collected for analysis of TMA-specific immunoglobulin. <i>Results:</i> Topical TMA exposure resulted in increased mRNA expression of proinflammatory and suppressive cytokines (IL-1β, TNF-α, IL-6, IFN-γ, IL-4, IL-10, IL-17, IL-23, TGF-β), chemokines (CXCL9, CXCL10, CCL24) and chemokine receptors (CCR7, CCR8, CXCR2), increased numbers of CD3+ T cells in ear tissue, and lymphadenopathy in the Smad3–/– mice. The IL-10 result was confirmed at the protein level by immunohistochemistry. However, the ear-swelling response and infiltration of eosinophils, F4/80+ cells, CD11c+ cells and mast cells were similar in the Smad3–/– mice compared to their wild-type (WT) siblings. While TMA-specific IgE was induced equally in the WT and Smad3–/– mice, the concentration of TMA-specific IgG2a was significantly lower in the Smad3–/– mice. <i>Conclusions:</i> The Smad3 molecule contributes significantly to the regulation of the cytokine and chemokine network during the CHS response to TMA. The lack of Smad3 resulted in a potent Th2 shift, confirmed by strongly impaired IgG2a levels.
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8.
  • Asarnoj, A, et al. (författare)
  • Anaphylaxis to peanut in a patient predominantly sensitized to Ara h 6
  • 2012
  • Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 159:2, s. 209-212
  • Tidskriftsartikel (refereegranskat)abstract
    • Diagnosis of peanut allergy has improved thanks to component-resolved diagnostics. Peanut allergen component Ara h 2 is considered to indicate true peanut allergy. The component Ara h 6 is structurally similar to Ara h 2, but the diagnostic value of analyzing IgE antibodies to Ara h 6 is unclear. A boy sensitized (≥0.35 kU<sub>A</sub>/l) to Ara h 8 but not to Ara h 1, Ara h 2 and Ara h 3 was challenged with peanut and developed grade II anaphylaxis. In serum collected at the time of challenge a doubling of IgE to the peanut allergen extract was observed compared to allergy testing 9 months earlier. In contrast, IgE levels to Ara h 1, Ara h 2, Ara h 3 and to Ara h 8 were rather unchanged. After another 2 months, Ara h 6 was analyzed and revealed a level of 24 kU<sub>A</sub>/l whilst Ara h 2 was 0.12 kU<sub>A</sub>/l. We suggest that IgE sensitization to Ara h 6 caused the reaction and conclude that analyses of IgE levels to peanut and peanut components should be performed in connection with a challenge. Furthermore, levels to Ara h 2 below 0.35 kU<sub>A</sub>/l may still indicate a risk of severe reaction at the time of challenge since in rare cases, Ara h 6 IgE antibodies may be present without occurrence of IgE antibodies to Ara h 2.
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9.
  • Asgardoon, MH, et al. (författare)
  • Monogenic Primary Immunodeficiency Disorder Associated with Common Variable Immunodeficiency and Autoimmunity
  • 2020
  • Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 181:9, s. 706-714
  • Tidskriftsartikel (refereegranskat)abstract
    • <b><i>Background:</i></b> Common variable immunodeficiency (CVID) is the most frequent primary immunodeficiency disorder mainly characterized by recurrent bacterial infections besides other immunological defects including loss of or dysfunction of B cells and decreased immunoglobulin levels. In this study, our aim is to evaluate clinical, immunological, and molecular data of patients with a primary clinical diagnosis of CVID and autoimmune phenotype with a confirmed genetic diagnosis. <b><i>Methods:</i></b> Among 297 patients with CVID, who were registered in the Iranian Primary Immunodeficiency Registry at Children’s Medical Center Hospital in Iran, 83 patients have been genetically examined and 27 patients with autoimmunity and confirmed genetic mutations were selected for analysis. Whole-exome sequencing and confirmatory Sanger sequencing methods were used for the study population. A questionnaire was retrospectively filled for all patients to evaluate demographic, laboratory, clinical, and genetic data. <b><i>Results:</i></b> In the 27 studied patients, 11 different genetic defects were identified, and the most common mutated gene was <i>LRBA</i>, reported in 17 (63.0%) patients. Two patients (7.7%) showed autoimmune complications as the first presentation of immunodeficiency. Eleven patients (40.7%) developed one type of autoimmunity, and 16 patients (59.3%) progressed to poly-autoimmunity. Most of the patients with mono-autoimmunity (<i>n</i> = 9, 90.0%) primarily developed infectious complications, while in patients with poly-autoimmunity, the most common first presentation was enteropathy (<i>n</i> = 6, 37.6%). In 13 patients (61.9%), the diagnosis of autoimmune disorders preceded the diagnosis of primary immunodeficiency. The most frequent autoimmune manifestations were hematologic (40.7%), gastrointestinal (48.1%), rheumatologic (25.9%), and dermatologic (22.2%) disorders. Patients with poly-autoimmunity had lower regulatory T cells than patients with mono-autoimmunity. <b><i>Conclusion:</i></b> In our cohort, the diagnosis of autoimmune disorders preceded the diagnosis of primary immunodeficiency in most patients. This association highlights the fact that patients referring with autoimmune manifestations should be evaluated for humoral immunity.
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10.
  • Azizi, G, et al. (författare)
  • Autoimmunity in Primary Antibody Deficiencies
  • 2016
  • Ingår i: International archives of allergy and immunology. - : S. Karger AG. - 1423-0097 .- 1018-2438. ; 171:3-4, s. 180-193
  • Tidskriftsartikel (refereegranskat)abstract
    • Primary antibody deficiencies (PADs) are the most common inherited primary immunodeficiencies in humans, characterized by hypogammaglobulinemia, an inability to produce specific antibodies, and recurrent infections mainly caused by encapsulated bacteria. However, it has been shown that inflammatory disorders, granulomatous lesions, lymphoproliferative diseases, cancer, and autoimmunity are associated with the various types of PAD. Both systemic and organ-specific autoimmune diseases could be attributed to B-cell defects in PAD patients. Immune thrombocytopenic purpura and autoimmune hemolytic anemia are the most common autoimmune disorders in this group of patients. The aim of this review is to describe the proposed mechanisms for autoimmunity and to review the literature with respect to the reported autoimmune disorders in each type of PAD.
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