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pubmed: 0091-6749



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Ozone exposure induces respiratory barrier biphasic injury and inflammation controlled by Interleukin-33.
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Ozone exposure induces respiratory barrier biphasic injury and inflammation controlled by Interleukin-33.

J Allergy Clin Immunol. 2018 Jan 10;:

Authors: Michaudel C, Mackowiak C, Maillet I, Fauconnier L, Akdis C, Sokolowska M, Dreher A, Tan HT, Quesniaux VF, Ryffel B, Togbe D

Abstract
BACKGROUND: IL-33 plays critical role in the regulation of tissue homeostasis, injury and repair. Whether IL-33 regulates neutrophil recruitment and function independently of airways hyperresponsiveness (AHR) in ozone induced lung injury and inflammation is unclear.
OBJECTIVE: To examine the role of IL-33/ST2 axis in lung inflammation upon acute ozone exposure in mice.
METHODS: ST2 and IL-33 deficient mice, IL-33-citrine reporter and C57BL/6 (WT) mice underwent a single ozone exposure (1 ppm for 1h) in all studies. Cell recruitment in lung and broncho-alveolar space, inflammatory parameters, epithelial barrier damage and airway hyperreactivity (AHR) were determined.
RESULTS: We report that a single ozone exposure causes a rapid disruption of the epithelial barrier within 1h followed by second phase of respiratory barrier injury with increased neutrophil recruitment, ROS production, AHR and IL-33 expression in epithelial and myeloid cells in WT mice. In the absence of IL-33 or IL-33R/ST2, epithelial cell injury with protein leak and myeloid cell recruitment and inflammation are further increased, while tight junction proteins E-cadherin and ZO-1, ROS expression in neutrophils and AHR are diminished. ST2 neutralization recapitulated the enhanced ozone induced neutrophilic inflammation. However, myeloid cell depletion using GR1 antibody reduced ozone induced lung inflammation, epithelial cell injury and protein leak, while administration of rmIL-33 reduced neutrophil recruitment in IL-33 deficient mice.
CONCLUSION: The data demonstrate that ozone causes an immediate barrier injury which precedes myeloid cell mediated inflammatory injury under the control of IL-33/ST2 axis. Thus, IL-33/ST2 signaling is critical for the maintenance of intact epithelial barrier and inflammation.

PMID: 29331644 [PubMed - as supplied by publisher]




Glucagon-like peptide 1 signaling inhibits allergen-induced lung IL-33 release and reduces group 2 innate lymphoid cell (ILC2) cytokine production in vivo.
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Glucagon-like peptide 1 signaling inhibits allergen-induced lung IL-33 release and reduces group 2 innate lymphoid cell (ILC2) cytokine production in vivo.

J Allergy Clin Immunol. 2018 Jan 10;:

Authors: Toki S, Goleniewska K, Reiss S, Zhang J, Bloodworth MH, Stier MT, Zhou W, Newcomb DC, Ware LB, Stanwood GD, Galli A, Boyd KL, Niswender KD, Peebles RS

Abstract
BACKGROUND: IL-33 is one of the most consistently associated gene candidates for asthma identified by GWAS. Studies in mice and in human cells have confirmed the importance of IL-33 in inducing type-2 cytokine production from both group 2 innate lymphoid cells (ILC2) and Th2 cells. However, there are no pharmacologic agents known to inhibit IL-33 release from airway cells.
OBJECTIVE: To determine the effect of glucagon like peptide receptor-1 GLP-1R signaling on aeroallergen-induced airway IL-33 production and release and on innate type-2 airway inflammation.
METHODS: BALB/c mice were challenged intranasally with Alternaria extract for 4 consecutive days. GLP-1R agonist or the vehicle was administered starting either 2 days before the first Alternaria extract-challenge or 1 day after the first Alternaria extract-challenge.
RESULTS: GLP-1R agonist treatment starting 2 days before the first Alternaria extract-challenge decreased IL-33 release in the BAL fluid and DUOX1 mRNA expression 1 h after the first Alternaria extract-challenge, and IL-33 expression in lung epithelial cells 24 h after the last Alternaria extract-challenge. Further, GLP-1R agonist significantly decreased the number of ILC2 expressing IL-5 and IL-13, the lung protein expression of type-2 cytokines and chemokines, the number of perivascular eosinophils, mucus production, and airway responsiveness compared with vehicle treatment. GLP-1R agonist treatment starting one day after the first Alternaria extract-challenge also significantly decreased eosinophilia and type-2 cytokine and chemokine expression in the airway after 4 days of Alternaria extract-challenge.
CONCLUSION: These results reveal that GLP-1R signaling may be a potential therapy to reduce IL-33 release and inhibit the ILC2 response to protease-containing aeroallergens, such as Alternaria.

PMID: 29331643 [PubMed - as supplied by publisher]




A functional splicing variant associated with decreased asthma risk abolishes the ability of gasdermin B (GSMDB) to induce epithelial cell pyroptosis.
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A functional splicing variant associated with decreased asthma risk abolishes the ability of gasdermin B (GSMDB) to induce epithelial cell pyroptosis.

J Allergy Clin Immunol. 2018 Jan 09;:

Authors: Panganiban RA, Sun M, Dahlin A, Park HR, Kan M, Himes BE, Mitchel JA, Iribarren C, Jorgenson E, Randell SH, Israel E, Tantisira K, Shore S, Park JA, Weiss ST, Wu AC, Lu Q

Abstract
BACKGROUND: Genetic variants in the chromosomal region 17q21 are consistently associated with asthma. However, mechanistic studies have not yet linked any of the associated variants to a function that could influence asthma, and as a result, the identity of the asthma gene(s) remains elusive.
OBJECTIVES: We sought to identify and characterize functional variants in the 17q21 locus.
METHODS: We used the Exome Aggregation Consortium (ExAC) browser to identify coding (amino acid-changing) variants in the 17q21 locus. We obtained asthma association measures for these variants in both the GERA cohort (16,274 cases and 38,269 matched controls) and the EVE Consortium study (5,303 asthma cases and 12,560 individuals). Gene expression and protein localization were determined by quantitative RT-PCR and fluorescence immunostaining, respectively. Molecular and cellular studies were performed to determine the functional effects of coding variants.
RESULTS: Two coding variants (rs2305480 and rs11078928) of the gasdermin B (GSDMB) gene in the 17q21 locus were associated with lower asthma risk in both GERA (OR = 0.92; P= 1.01 × 10-6) and EVE (OR= 0.85; Joint PEVE = 1.31 ×10-13). In GERA, rs11078928 had a minor allele frequency (MAF) of 0.45 in unaffected (non-asthmatic) controls and 0.43 in asthma cases. For European Americans in EVE the MAF of rs2305480 was 0.45 for controls and 0.39 for cases; for all EVE subjects the MAF was 0.32 for controls and 0.27 for cases. GSDMB is highly expressed in differentiated airway epithelial cells, including the ciliated cells. We found that when the GSDMB protein is cleaved by inflammatory caspase-1 to release its N-terminal fragment, potent pyroptotic cell death was induced. The splicing variant rs11078928 deletes the entire exon 6, which encodes 13 amino acids in the critical N-terminus, and abolishes the pyroptotic activity of the GSDMB protein.
CONCLUSIONS: Our study identified a functional asthma variant in the GSDMB gene of the 17q21 locus and implicates GSDMB-mediated epithelial cell pyroptosis in pathogenesis.

PMID: 29330013 [PubMed - as supplied by publisher]




Basophil testing with CD63 in pollen sensitised patients is independent of the circadian clock.
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Basophil testing with CD63 in pollen sensitised patients is independent of the circadian clock.

J Allergy Clin Immunol. 2018 Jan 09;:

Authors: Lind C, Skaarup SH, Lorentz A, Hoffmann HJ

PMID: 29330012 [PubMed - as supplied by publisher]




Mutations in PI3K110δ cause impaired NK cell function partially rescued by rapamycin treatment.
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Mutations in PI3K110δ cause impaired NK cell function partially rescued by rapamycin treatment.

J Allergy Clin Immunol. 2018 Jan 09;:

Authors: Ruiz-García R, Vargas-Hernandez A, Chinn IK, Angelo LS, Cao TN, Coban-Akdemir Z, Jhangiani SN, Meng Q, Forbes LR, Muzny DM, Allende LM, Ehlayel MS, Gibbs RA, Lupski JR, Uzel G, Orange JS, Mace EM

Abstract
BACKGROUND: Heterozygous gain-of-function mutations in PI3K110 lead to lymphadenopathy, lymphoid hyperplasia, Epstein-Barr virus (EBV) and cytomegalovirus (CMV) viremia, and sinopulmonary infections.
OBJECTIVE: The known role of NK cell function in the control of EBV and CMV prompted us to investigate the functional and phenotypic effect of PI3K110δ mutations on NK cell subsets and cytotoxic function.
METHODS: Patient mutations were identified by whole exome or targeted sequencing. We performed NK cell phenotyping and functional analysis of patient cells by flow cytometry, standard Cr51 cytotoxicity assays, and quantitative confocal microscopy.
RESULTS: PI3K110δ mutations led to an altered NK cell developmental phenotype and cytotoxic dysfunction. Impaired NK cell cytotoxicity was due to decreased conjugate formation with susceptible target cells and abrogated activation of cell machinery required for target cell killing. These defects were partially restored following the initiation of treatment with rapamycin in three patients.
CONCLUSION: We describe novel NK cell functional deficiency due to PI3K110δ mutation, which is a likely contributor to the severe viremia observed in these patients. Rapamycin treatment partially restores NK cell function, providing further rationale for its use in this disease.

PMID: 29330011 [PubMed - as supplied by publisher]




Nasopharyngeal Lactobacillus is Associated with Childhood Wheezing Illnesses Following Acute Respiratory Syncytial Virus Infection in Infancy.
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Nasopharyngeal Lactobacillus is Associated with Childhood Wheezing Illnesses Following Acute Respiratory Syncytial Virus Infection in Infancy.

J Allergy Clin Immunol. 2018 Jan 09;:

Authors: Rosas-Salazar C, Shilts MH, Tovchigrechko A, Schobel S, Chappell JD, Larkin EK, Gebretsadik T, Halpin RA, Nelson KE, Moore ML, Anderson LJ, Peebles RS, Das SR, Hartert TV

Abstract
BACKGROUND: Early-life acute respiratory infection (ARI) with respiratory syncytial virus (RSV) has been strongly associated with the development of childhood wheezing illnesses, but the pathways underlying this association are poorly understood.
OBJECTIVE: To examine the role of the nasopharyngeal microbiome in the development of childhood wheezing illnesses following RSV ARI in infancy.
METHODS: We conducted a nested cohort study of 118 previously healthy, term infants with confirmed RSV ARI by RT-PCR. We used next-generation sequencing of the V4 region of the 16S rRNA gene to characterize the nasopharyngeal microbiome during RSV ARI. Our main outcome of interest was 2-year subsequent wheeze.
RESULTS: One hundred thirteen (95.8%) of the 118 infants had 2-year outcome data. Of these, 46 (40.7%) had parental report of subsequent wheeze. There was no association between the overall taxonomic composition, diversity, and richness of the nasopharyngeal microbiome during RSV ARI with the development of subsequent wheeze. However, the nasopharyngeal detection and abundance of Lactobacillus was consistently higher in infants who did not develop this outcome. Lactobacillus also ranked first among the different genera in a model distinguishing infants with and without subsequent wheeze.
CONCLUSION: The nasopharyngeal detection and increased abundance of Lactobacillus during RSV ARI in infancy are associated with a reduced risk of childhood wheezing illnesses at age 2 years.

PMID: 29330010 [PubMed - as supplied by publisher]




The call for considering follicular helper T cells in IgG4-related disease.
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The call for considering follicular helper T cells in IgG4-related disease.

J Allergy Clin Immunol. 2018 Jan 09;:

Authors: Akiyama M

PMID: 29329900 [PubMed - as supplied by publisher]




Reply.
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Reply.

J Allergy Clin Immunol. 2018 Jan 09;:

Authors: Karim AF, Heeringa JJ, van Laar JAM, Verdijk RM, Dik WA, Paridaens AD, van Hagen PM, van Zelm MC

PMID: 29329899 [PubMed - as supplied by publisher]




Canadian genome-wide association study and meta-analysis confirm HLA as a risk factor for peanut allergy independent of asthma.
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Canadian genome-wide association study and meta-analysis confirm HLA as a risk factor for peanut allergy independent of asthma.

J Allergy Clin Immunol. 2018 Jan 08;:

Authors: Asai Y, Eslami A, van Ginkel CD, Akhabir L, Wan M, Yin D, Ellis G, Ben-Shoshan M, Marenholz I, Martino D, Ferreira MA, Allen K, Mazer B, de Groot H, de Jong NW, Gerth van Wijk R, Dubois AEJ, Grosche S, Ashley S, Rüschendorf F, Kalb B, Beyer K, Nöthen MM, Lee YA, Chin R, Cheuk S, Hoffman J, Jorgensen E, Witte JS, Melles RB, Hong X, Wang X, Hui J, Musk AWB, Hunter M, James AL, Koppelman GH, Sandford AJ, Clarke AE, Daley D

PMID: 29325868 [PubMed - as supplied by publisher]




Effects of Rhinovirus (RV) 39 Infection on Airway Hyper-responsiveness (AHR) to Carbachol in Human Airways Precision Cut Lung Slices (PCLS).
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Effects of Rhinovirus (RV) 39 Infection on Airway Hyper-responsiveness (AHR) to Carbachol in Human Airways Precision Cut Lung Slices (PCLS).

J Allergy Clin Immunol. 2018 Jan 06;:

Authors: Kennedy JL, Koziol-White CJ, Jeffus S, Rettiganti MR, Fisher P, Kurten M, Eze A, House S, Sikes JD, Askew E, Putt C, Panettieri RA, Jones SM, Kurten RC

PMID: 29317243 [PubMed - as supplied by publisher]




Role of airway glucose in bacterial infections in patients with chronic obstructive pulmonary disease.
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Role of airway glucose in bacterial infections in patients with chronic obstructive pulmonary disease.

J Allergy Clin Immunol. 2017 Dec 13;:

Authors: Mallia P, Webber J, Gill SK, Trujillo-Torralbo MB, Calderazzo MA, Finney L, Bakhsoliani E, Farne H, Singanayagam A, Footitt J, Hewitt R, Kebadze T, Aniscenko J, Padmanaban V, Molyneaux PL, Adcock IM, Barnes PJ, Ito K, Elkin SL, Kon OM, Cookson WO, Moffat MF, Johnston SL, Tregoning JS

Abstract
BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) have increased susceptibility to respiratory tract infection, which contributes to disease progression and mortality, but mechanisms of increased susceptibility to infection remain unclear.
OBJECTIVES: The aim of this study was to determine whether glucose concentrations were increased in airway samples (nasal lavage fluid, sputum, and bronchoalveolar lavage fluid) from patients with stable COPD and to determine the effects of viral infection on sputum glucose concentrations and how airway glucose concentrations relate to bacterial infection.
METHODS: We measured glucose concentrations in airway samples collected from patients with stable COPD and smokers and nonsmokers with normal lung function. Glucose concentrations were measured in patients with experimentally induced COPD exacerbations, and these results were validated in patients with naturally acquired COPD exacerbations. Relationships between sputum glucose concentrations, inflammatory markers, and bacterial load were examined.
RESULTS: Sputum glucose concentrations were significantly higher in patients with stable COPD compared with those in control subjects without COPD. In both experimental virus-induced and naturally acquired COPD exacerbations, sputum and nasal lavage fluid glucose concentrations were increased over baseline values. There were significant correlations between sputum glucose concentrations and sputum inflammatory markers, viral load, and bacterial load. Airway samples with higher glucose concentrations supported more Pseudomonas aeruginosa growth in vitro.
CONCLUSIONS: Airway glucose concentrations are increased in patients with stable COPD and further increased during COPD exacerbations. Increased airway glucose concentrations might contribute to bacterial infections in both patients with stable and those with exacerbated COPD. This has important implications for the development of nonantibiotic therapeutic strategies for the prevention or treatment of bacterial infection in patients with COPD.

PMID: 29310905 [PubMed - as supplied by publisher]




Minimally invasive skin tape strip RNA-seq identifies novel characteristics of type 2-high atopic dermatitis disease endotype.
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Minimally invasive skin tape strip RNA-seq identifies novel characteristics of type 2-high atopic dermatitis disease endotype.

J Allergy Clin Immunol. 2018 Jan 05;:

Authors: Dyjack N, Goleva E, Rios C, Kim BE, Bin L, Taylor P, Bronchick C, Hall CF, Richers BN, Seibold MA, Leung DY

Abstract
BACKGROUND: Expression profiling of skin biopsies has established molecular features of the skin in atopic dermatitis (AD). Invasiveness of biopsies has prevented their use in defining individual level AD pathobiological mechanisms (endotypes) in large research studies.
OBJECTIVE: To determine if minimally invasive skin tape strip transcriptome analysis identifies gene expression dysregulation in AD and molecular disease endotypes.
METHODS: We sampled non-lesional and lesional skin tape strips and biopsies from adult Caucasian subjects AD patients (18 males, 12 females; age (Mean±SE) 36.3±2.2 yrs) and healthy controls (9 males, 16 females; age (Mean±SE) 34.8±2.2 yrs). Ampliseq whole transcriptome sequencing was performed on extracted RNA. Differential expression, clustering/pathway analyses, immunostaining of skin biopsies, and clinical trait correlations were performed.
RESULTS: Skin tape expression profiles were distinct from skin biopsy profiles and better sampled epidermal differentiation complex genes. Skin tape expression of 29 immune and epidermis-related genes (FDR<5%) separated AD from healthy subjects. Agnostic gene set analyses and clustering revealed 50% of AD subjects exhibited a type 2 inflammatory signature (type 2-high endotype) characterized by differential expression of 656 genes including overexpression of IL13, IL4R, CCL22, CCR4 (log2FC=5.5, 2.0, 4.0, and 4.1, respectively), and at a pathway level by T-helper 2/dendritic cell activation. Both expression and immunostaining of skin biopsies indicated this type 2-high group was enriched for inflammatory, type 2-skewed dendritic cells expressing the high affinity IgE receptor (FcεRI). The type 2-high endotype group exhibited more severe disease by both EASI score and body surface area covered by lesions.
CONCLUSION: Minimally invasive expression profiling of non-lesional skin reveals stratification in AD molecular pathology by type 2 inflammation that correlates with disease severity.

PMID: 29309794 [PubMed - as supplied by publisher]




A Decade of Research on the 17q12-21 Asthma Locus: Piecing Together the Puzzle.
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A Decade of Research on the 17q12-21 Asthma Locus: Piecing Together the Puzzle.

J Allergy Clin Immunol. 2018 Jan 04;:

Authors: Stein MM, Thompson EE, Schoettler N, Helling BA, Magnaye KM, Stanhope C, Igartua C, Morin A, Washington C, Nicolae D, Bønnelykke K, Ober C

Abstract
Chromosome 17q12-21 remains the most highly replicated and significant asthma locus. Genotypes in the core region defined by the first GWAS correlate with expression of two genes, ORMDL3 and GSDMB, making these prime candidate asthma genes, although recent studies have implicated GSDMA distal to and PGAP3 proximal to the core region as independent loci. We review here 10 years of studies on the 17q12-21 locus and suggest that genotype-specific risks for asthma at the proximal and distal loci are not specific to early onset asthma and mediated by PGAP3, ORMDL3, and/or GSDMA expression. We propose that the weak and inconsistent associations of 17q SNPs with asthma in African Americans is due to the high frequency of some 17q alleles, the breakdown of linkage disequilibrium on African-derived chromosomes, and possibly different early life asthma endotypes in these children. Finally, the inconsistent association between asthma and gene expression levels in blood or lung cells from older children and adults suggests that genotype effects may mediate asthma risk or protection during critical developmental windows and/or in response to relevant exposures in early life. Thus, studies of young children and ethnically diverse populations are required to fully understand the relationship between genotype and asthma phenotype and the gene regulatory architecture at this locus.

PMID: 29307657 [PubMed - as supplied by publisher]




Food allergy and omics.
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Food allergy and omics.

J Allergy Clin Immunol. 2018 Jan;141(1):20-29

Authors: Dhondalay GK, Rael E, Acharya S, Zhang W, Sampath V, Galli SJ, Tibshirani R, Boyd SD, Maecker H, Nadeau KC, Andorf S

Abstract
Food allergy (FA) prevalence has been increasing over the last few decades and is now a global health concern. Current diagnostic methods for FA result in a high number of false-positive results, and the standard of care is either allergen avoidance or use of epinephrine on accidental exposure, although currently with no other approved treatments. The increasing prevalence of FA, lack of robust biomarkers, and inadequate treatments warrants further research into the mechanism underlying food allergies. Recent technological advances have made it possible to move beyond traditional biological techniques to more sophisticated high-throughput approaches. These technologies have created the burgeoning field of omics sciences, which permit a more systematic investigation of biological problems. Omics sciences, such as genomics, epigenomics, transcriptomics, proteomics, metabolomics, microbiomics, and exposomics, have enabled the construction of regulatory networks and biological pathway models. Parallel advances in bioinformatics and computational techniques have enabled the integration, analysis, and interpretation of these exponentially growing data sets and opens the possibility of personalized or precision medicine for FA.

PMID: 29307411 [PubMed - in process]




Mechanisms of food allergy.
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Mechanisms of food allergy.

J Allergy Clin Immunol. 2018 Jan;141(1):11-19

Authors: Sampson HA, O'Mahony L, Burks AW, Plaut M, Lack G, Akdis CA

Abstract
Although oral tolerance is the normal physiologic response to ingested antigens, a breakdown in this process appears to have occurred in the past 2 decades, leading to an increasing prevalence of sensitization to food allergens. Over the past decade, basic research has intensified in an attempt to better understand the mechanisms leading to sensitization and disease versus desensitization and short- and long-term tolerance. In this review we assess various factors that can influence tissue and immune responses to food antigens, the current understanding of immune tolerance development, the role of the gastrointestinal microbiota, and current knowledge regarding immunologic mechanisms involved in desensitization and sustained unresponsiveness, although perhaps the latter is more appropriately termed remission.

PMID: 29307410 [PubMed - in process]




Treatment for food allergy.
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Treatment for food allergy.

J Allergy Clin Immunol. 2018 Jan;141(1):1-9

Authors: Burks AW, Sampson HA, Plaut M, Lack G, Akdis CA

Abstract
The prevalence of IgE-mediated food allergy is an increasing public health concern effecting millions of persons worldwide. The current standard of treatment is strict avoidance of the offending food or foods, and to date, there are no regulatory approved treatments for food allergy. A significant amount of research has been directed at various forms of food immunotherapy, including oral, sublingual, and epicutaneous delivery routes. Although oral immunotherapy has shown the greatest promise for efficacy in terms of the amount of protein that can be ingested, it has also demonstrated less tolerability and a less favorable safety profile compared with sublingual immunotherapy and epicutaneous immunotherapy, which offers the least protection but has the best safety and tolerability profile. Studies have been conducted with adding adjuvants and anti-IgE to enhance either the efficacy or safety of food immunotherapy. Multiple concepts of food immunotherapy beyond these first-generation treatments are in either animal or early phase 1 studies.

PMID: 29307409 [PubMed - in process]




High-quality assembly of Dermatophagoides pteronyssinus genome and transcriptome reveals a wide range of novel allergens.
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High-quality assembly of Dermatophagoides pteronyssinus genome and transcriptome reveals a wide range of novel allergens.

J Allergy Clin Immunol. 2018 Jan 02;:

Authors: Liu XY, Yang KY, Wang MQ, Kwok JS, Zeng X, Yang Z, Xiao XJ, Lau CP, Li Y, Huang ZM, Ba JG, Yim AK, Ouyang CY, Ngai SM, Chan TF, Leung EL, Liu L, Liu ZG, Tsui SK

PMID: 29305317 [PubMed - as supplied by publisher]




Endogenous and exogenous sex steroid hormones in asthma and allergy in females: a systematic review and meta-analysis.
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Endogenous and exogenous sex steroid hormones in asthma and allergy in females: a systematic review and meta-analysis.

J Allergy Clin Immunol. 2018 Jan 02;:

Authors: McCleary N, Nwaru BI, Nurmatov UB, Critchley H, Sheikh A

PMID: 29305316 [PubMed - as supplied by publisher]




RELA haploinsufficiency in CD4 lymphoproliferative disease with autoimmune cytopenias.
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RELA haploinsufficiency in CD4 lymphoproliferative disease with autoimmune cytopenias.

J Allergy Clin Immunol. 2018 Jan 02;:

Authors: Comrie WA, Faruqi AJ, Price S, Zhang Y, Rao VK, Su HC, Lenardo MJ

PMID: 29305315 [PubMed - as supplied by publisher]