HLA and asthma phenotypes/endotypes: A review

Kontakioti, Eirini; Domvri, Kalliopi; Papakosta, Despina; Daniilidis, M.

doi:10.1016/j.humimm.2014.06.022

Cited by 57 publications

(43 citation statements)

References 110 publications

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“…HLA-DRB1*04 has already been associated with aspirin-induced asthma [37], and HLA-DPB1 has been reported to be the most relevant marker of this phenotype [60]. We did not find an association with this allele in our cohort.…”

Section: Discussioncontrasting

confidence: 63%

Allergic and Nonallergic Asthma Have Distinct Phenotypic and Genotypic Features

Takejima

Agondi²,

Rodrigues³

et al. 2017

Int Arch Allergy Immunol

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Background: Identification of asthma phenotypes enables a better understanding and management of this heterogeneous disease. Studies have reported associations between human leukocyte antigens (HLA) and asthma in different populations, but the results have been inconclusive and they have rarely considered the distinct disease phenotypes. Our objective was to characterize allergic and nonallergic asthma phenotypes and evaluate possible associations with the HLA system. Methods: A total of 109 patients with asthma were prospectively followed during 2 years. They were divided into 2 groups, i.e., allergic and nonallergic asthma, according to their clinical history and skin prick test and serum-specific immunoglobulin E (IgE) results. The control group comprised 297 deceased donors of solid organs. Patients' features and HLA class I and II genotypes were assessed and compared. Results: This study showed different features between asthma phenotypes. Nonallergic patients were older at the onset of asthma symptoms and had a higher rate of intolerance to nonsteroidal anti-inflammatory drugs. Allergic patients had higher total serum IgE levels, reported atopic dermatitis and rhinoconjunctivitis more frequently, and, unexpectedly, had a greater disease severity. New associations between the HLA genotypes and allergic and nonallergic asthma were identified. The HLA-B*42, HLA-C*17, HLA-DPA1*03, and HLA-DPB1*105 genotypes were associated with allergic asthma and the HLA-B*48 genotype with the nonallergic phenotype. The presence of the haplotype HLA-DPA1*03 DQA*05 was associated with allergic asthma, and the presence of HLA-DPA1*03 and the absence of HLA-DQA*05 with nonallergic asthma. Conclusions: Allergic and nonallergic asthma have distinct phenotypic and genotypic features. New associations between asthma phenotypes and HLA class I and II were identified.

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Section: Discussioncontrasting

confidence: 63%

Allergic and Nonallergic Asthma Have Distinct Phenotypic and Genotypic Features

Takejima

Agondi²,

Rodrigues³

et al. 2017

Int Arch Allergy Immunol

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“…Tsuji et al (10) found significantly higher serum IgE and urinary leukotriene E4 levels at HSP onset and also found IgE deposits in Langerhans and mast cells in patients with HSP nephritis. These findings implied that the stimulation of IgE-sensitized mast cells by specific antigens in the presence of IgA circulating immune complexes might increase capillary permeability and perivascular deposition of IgA circulating immune complexes in the small vessels of the skin and renal glomeruli (10,22). Kawasaki et al (14) found elevated serum IL-4 levels in patients with acute HSP without nephritis as well as IL-5 and ECP-activated eosinophils at the onset of HSP nephritis.…”

Section: Hsp In Allergic Diseasesmentioning

confidence: 97%

“…Davin et al (12) reported that the incidence of increased plasma IgE levels relative to age-matched normal values was significantly higher among HSP patients, indicating that IgE may play a pathogenic role in HSP. IL-5 induces B-cell immunoglobulin class switching to IgA and also activates eosinophils (22)(23)(24). HSP has previously been considered an IgA-mediated vasculitis (1).…”

Section: Hsp In Allergic Diseasesmentioning

confidence: 99%

“…The authors concluded that the functional imbalance in Th cell subsets and aberrant Th2 and Th17 activation might be associated with the aberrant antibody production and vasculitis development (20). Epidemiological data reveal that the prevalence of Th1-mediated autoimmune diseases has been rising in parallel with Th2-mediated allergic diseases worldwide over the past two decades (21)(22)(23). The hygiene hypothesis suggests that early-life infections and microbial exposures may protect against the development of allergy and autoimmune diseases, as a potential explanation for the increased occurrence of allergic and autoimmune diseases (24)(25)(26).…”

Section: Hsp In Allergic Diseasesmentioning

confidence: 99%

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Association between allergic diseases and risks of HSP and HSP nephritis: a population-based study

et al. 2015

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Background: Some allergic inflammation-associated mediators have been reported in acute stage of HenochSchönlein purpura (HSP). However, the association of children with allergic diseases and their subsequent risks of HSP and HSP nephritis remain unknown. Methods: In this study, we included 2,240 children with HSP diagnosed between 2000 and 2008 as well as 8,960 non-HSP controls matched for age, sex, and level of urbanization. The odds ratios (ORs) of HSP were calculated with respect to associations with pre-existing allergic diseases. results: Children with allergic diseases had an increased subsequent risk of HSP; the lowest adjusted OR (aOR) was 1.33 for allergic conjunctivitis (95% confidence interval (CI): 1.17-1.52) and the highest was 1.68 for asthma (95% CI: 1.48-1.91). The aOR increased to 2.03 (95% CI: 1.80-2.31) in children with at least two allergic diseases. Children who visited medical institutes more often per year for associated allergic diseases had an increased risk of HSP. Of the 2,240 children with HSP, 249 (11%) had HSP nephritis and 45.8% of those with nephritis had history of any allergic disease. conclusion: Atopic children had an increased subsequent risk of HSP but not an increased risk of HSP nephritis. h enoch-Schönlein purpura (HSP) is a common systemic small vessel vasculitis that primarily affects children and is characterized by nonthrombocytopenic purpura, abdominal pain and bleeding, arthritis, and renal involvement. Although the clinical course of HSP is generally benign and self-limited (1), renal function impairment, bowel perforation, and central nerve system involvement are rare but cause severe morbidity and long-term complication which need more aggressive treatment (1-3). HSP with renal involvement, HSP nephritis, has been reported to occur in 20-50% of the patients with HSP, and the long-term outcome of HSP depends primarily on the extent of renal involvement (4-7). The manifestations of HSP nephritis vary from asymptomatic hematuria and/or proteinuria to nephritic syndrome, nephrotic syndrome, and rapidly progressive glomerulonephritis (4-7). To date, the exact etiology and pathogenesis of HSP are unknown. However, HSP is regarded as a specific immune-mediated inflammation induced by environmental factors, such as infections and seasonal variation (1,8). Some inflammatory mediators, including tumor necrosis factor (TNF)-α, interleukin-6, IL-8, transforming growth factor (TGF)-β, vascular endothelial growth factor (VEGF), and cysteinyl leukotrienes, have been reported to be higher in children with acute HSP than in healthy controls (9-11). Cysteinyl leukotrienes are potent inflammatory mediators which contribute to asthma (12). Elevated Th2-mediated biological markers such as elevated serum IgE, serum eosinophil cationic protein (ECP), and urinary leukotriene E4 levels were found in acute stage of HSP (10-13). The onset of HSP has been reported after exposure to drug or food allergens, vaccines, and insect bites (14-16). In our clinical experience, some children with HS...

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“…The GWAS revealed that this gene region accounted for approximately 20% of PA in the study population [42]. Previous studies that associated mutations in HLA genes with PA and other autoimmune disorders confirm the biological credibility of these finding [51][52][53][54]. Although a strong genetic base for PA has been identified via GWAS, it is also clear that genetics is neither sufficient nor causative for development of the allergy as not all participants with the identified genetic risk factor developed PA.…”

Section: Epigenetic Mediation Of Genetic Susceptibilitymentioning

confidence: 77%