Abstract Background Chlorhexidine (CHX) is a widely utilized disinfectant that can cause IgE‐mediated urticaria/anaphylaxis. The cross‐reactivity of patients with IgE‐mediated CHX‐allergy with other disinfectants, which share structural similarities with CHX like polyhexanide (polyhexamethylene biguanide; PHMB), alexidine (ALX) or octenidine (OCT) is unknown. Methods 44 patients with anaphylaxis or urticaria upon CHX exposure and positive skin prick test (SPT) and/or positive CHX ImmunoCAP...
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Publication date: Available online 18 July 2020Source: Journal of Allergy and Clinical ImmunologyAuthor(s): Zhaozhong Zhu, Kohei Hasegawa, Carlos A. Camargo, Liming Liang
Publication date: Available online 18 July 2020Source: Journal of Allergy and Clinical ImmunologyAuthor(s): Rachel L. Peters, Danny Ye Barret, Victoria X. Soriano, Vicki McWilliam, Adrian J. Lowe, Anne-Louise Ponsonby, Mimi L.K. Tang, Shyamali C. Dharmage, Lyle C. Gurrin, Jennifer J. Koplin, Kirsten P. Perrett
Publication date: Available online 18 July 2020Source: Journal of Allergy and Clinical ImmunologyAuthor(s): Andréanne Morin, Chris G. McKennan, Casper-Emil T. Pedersen, Jakob Stokholm, Bo L. Chawes, Ann-Marie Malby Schoos, Katherine A. Naughton, Jonathan Thorsen, Martin S. Mortensen, Donata Vercelli, Urvish Trivedi, Søren J. Sørensen, Hans Bisgaard, Dan L. Nicolae, Klaus Bønnelykke, Carole Ober
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Many abrupt adjustments in the delivery of medical care became necessary due to the unexpected emergence of the COVID-19 pandemic in early 2020. In order to ensure social distancing and the concomitant requirements for personal protective equipment, practitioners have had to make a myriad of adjustments in order to continue providing subcutaneous allergen immunotherapy (SCIT). In many practices SCIT was stopped or administration intervals have been increased, while other practices have transitioned...
The COVID-19 pandemic has caused high utilization of healthcare resources including hospitalization and intensive care unit treatment. There has been considerable interest in determining which clinical factors stratify patients into high or low risk for severe COVID-19 illness to aid with clinical decision making. Advanced age, cardiovascular disease and diabetes have been associated with increased COVID-19 severity1. Asthma appears to be under-represented as a COVID-19 comorbidity compared to its...
Sensitization to nickel (Ni2+) is the most common type IV immune response, with estimates that 17% of women and 3% of men are nickel-sensitized1; likely an underestimate due to unreported cases. The route and timing of nickel exposure drive sensitization. Higher rates (12.2%)2, established by patch testing, are associated with early exposure through piercings i.e. skin and blood; early exposure orally through braces had Ni2+-sensitization rates similar to baseline (2.9%). As higher dermal exposure...
Intravenous recombinant enzyme replacement therapy (ERT) is currently available for eight lysosomal diseases. Hypersensitivity reactions (HSR) may be observed during this long-term treatment.
Electronic health record (EHR) data have become a major tool for clinical research. EHRs allow researchers to use computable phenotypes, which utilize a computerized query of data elements and logical rules to identify a cohort in the EHR. Given the complexity of EHR data, it is important that computable phenotypes be well validated. The limited computable phenotype literature in asthma has relied on encounter-based criteria, wherein individuals are only included if they have had encounter(s) with...
Atopic diseases worsen with psychological stress, but how stress contributes to their pathogenesis is still not clear. We review the evidence supporting the premise that stress contributes to allergic and inflammatory processes via stimulation of mast cells (MC) by neuroimmune stimuli.
Complement factor I (CFI) deficiency is a rare disorder with 38 reported cases worldwide(1). The immune system has adaptive and innate pathways. The complement system is part of the innate pathway, which through proteolytic reactions, clears immune complexes and opsonizes and kills microbial pathogens (2). There are three independent pathways of complement activation: classical, alternative, and lectin that converge at a common pathway to activate C3.
The National Institute for Allergy and Infectious Disease 2017 guidelines’ recommendation for early testing and introduction of peanut for at-risk infants has led to increased demand for practitioners to offer skin prick testing (SPT) and oral food challenges (OFC) to infants as young as 4 months of age.1 Data from clinical trials2,3,4 and population-based studies5,6 suggest that severe reactions and epinephrine use during infant OFC are uncommon. Safety data for infant OFC performed in clinical...
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Publication date: Available online 18 July 2020Source: Autoimmunity ReviewsAuthor(s): Aaron Lerner, Torsten Matthias
Publication date: Available online 17 July 2020Source: Autoimmunity ReviewsAuthor(s): Elisa Tinazzi, Nicola Osti, Ruggero Beri, Giuseppe Argentino, Dino Veneri, Francesco Dima, Caterina Bason, Gnaneshwer Jadav, Marzia Dolcino, Antonio Puccetti, Claudio Lunardi
Publication date: Available online 16 July 2020Source: Autoimmunity ReviewsAuthor(s): Maria Letizia Urban, Alessandra Bettiol, Caterina Serena, Chiara Comito, Irene Turrini, Silvia Fruttuoso, Elena Silvestri, Alfredo Vannacci, Claudia Ravaldi, Felice Petraglia, Giacomo Emmi, Domenico Prisco, Federico Mecacci
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Background Interleukin 13 (IL‐13) is a pleiotropic cytokine that has been shown to be important in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) and other type 2 inflammation–related diseases. Increased IL‐13 expression can elicit several pro‐inflammatory effects, including eosinophilia, and pathology such as increased mucus secretion. Polypogenesis in chronic rhinosinusitis (CRS) can be caused by hypoxia, which can also lead to hyperpermeability of airway epithelium and...
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Publication date: Available online 18 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Yan Zhang, Kirsten M. Anderson, Brian M. Freed, Shaodong Dai, Karin A. Pacheco
Publication date: Available online 18 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Anjeni Keswani, Klodian Dhana, Jamie A. Rosenthal, Donyea Moore, Mahboobeh Mahdavinia
Publication date: Available online 18 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Désirée Larenas-Linnemann, Tolly Epstein, Punita Ponda, David Bernstein, Paul Williams, Peter Creticos
Publication date: Available online 17 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Ravneet Donegan, Sonia Mathew, Alan P. Knutsen
Publication date: Available online 17 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Angela Chan, Elizabeth Feuille, Edith Schussler
Publication date: Available online 17 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Theoharis C. Theoharides
Publication date: Available online 17 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Irem Turgay Yagmur, Ozlem Unal Uzun, Aynur Kucukcongar Yavas, Ilknur Kulhas Celik, Muge Toyran, Mehmet Gunduz, Ersoy Civelek, Emine Dibek Misirlioglu
Publication date: Available online 17 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Monica Tang, Benjamin A. Goldstein, Jingye He, Jillian H. Hurst, Jason E. Lang
Publication date: Available online 16 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Stanley Fineman, Vivian Hernandez-Trujillo, Gerald B. Lee
Publication date: Available online 16 July 2020Source: Annals of Allergy, Asthma & ImmunologyAuthor(s): Mindy R. Hong, Donald Lei, Muhammad Yousaf, Rajeev Chavda, Sylvie Gabriel, Sherief R. Janmohamed, Jonathan I. Silverberg
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Coronavirus disease-2019 (COVID-19) is caused by the newly emerged virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and was recently declared as a pandemic by the World Health Organization. In its severe form, the disease is characterized by acute respiratory distress syndrome, and there are no targeted intervention strategies to treat or prevent it. The immune response is thought to both contribute to the pathogenesis of disease and provide protection during its resolution. Thus,...
Key Points Soluble but not crystalline UA acts as a negative regulator of innate immunity. sUA suppresses activated monocytes via SLC2A9-mediated intracellular uptake. Asymptomatic HU attenuates MSU crystal–induced tissue inflammation.
Key Points Blockade of Ly49/MHC-I interactions by anti–MHC-I results in the activation of NK cells. IFN- produced by activated NK cells stimulates APC to produce IL-15. Activated NK and T cells markedly augment antiviral and antitumor immunity.
Key Points Disparate selection occurs with age upon B-1a cells with different specificities. Disparate selection occurs with age upon B-1a cells in distinct locations.
Key Points MHC I can be induced in skeletal muscle in a doxycycline dose–dependent manner. Elevated muscle MHC I results in initial enhanced immune control of Trypanosoma cruzi. Sustained elevation in muscle MHC I ultimately exhausts pathogen-specific responses.
Key Points We identify checkpoints restricting the BCR-induced class switch recombination. TRAF3 maintains B cell homeostasis by fine-tuning the BCR signaling strength.
Key Points LPS increases cell surface expression of the SE receptor CRT. SE–CRT interaction increases [Ca2+], PAD activation, and protein citrullination. In SE-expressing Tg mice, LPS activates PAD, ACPA, and bone erosions.
Key Points A murine IL-17F.S65L ortholog recapitulates the impaired signaling function in vitro. IL-17F.S65L knock-in mice are susceptible to oral candidiasis, unlike Il17f–/– mice. Il17fS65L/S65L mice may be a broadly valuable tool to interrogate IL-17F function.
Key Points HIV RPs are an understudied patient population. Globally, IgG SHM is inversely correlated with disease progression. Longitudinal lineage tracking reveals ongoing SHM with disrupted selection in RPs.
Key Points The cell surface receptors RAGE and TLR4 regulate HMGB1-induced inflammation. RAGE promotes TLR4 trafficking to the cell surface but does not affect its translation. TLR4 regulates the translation of RAGE, which translocates to the cell surface.
Key Points lncRNA BCALM (AC099524.1) is B cell specific and highly expressed in human lymphomas. BCALM is necessary for the interaction of signal transduction proteins PLD1 and AKAP9. BCALM promotes negative feedback that downmodulates BCR-stimulated Ca+ signaling.
Key Points L. paracasei inhibits NLRP3 inflammasome activation in vitro. The inhibitory effect of L. paracasei on the inflammasome is dependent on IL-10. Oral administration of L. paracasei prevents inflammation-related disorders.
Key Points Dendritic cells transfer Ags to and activate B cells in vivo. Ags released from dendritic cells by regurgitation promote B cell activation. Early B cell activation by dendritic cell regurgitation requires NF-B/cRel.
Key Points ILC3-derived LT and IEC-derived LTβR regulate innate defense against Listeria. LT–LTβR axis increases GC numbers and MUC2 expression during Listeria infection. LTβR signaling and downstream RelB are associated with GC differentiation.
Key Points Glucocorticoid binding to glucocorticoid receptors in B cells upregulates CXCR4. Glucocorticoids control diurnal exchange of B cells between blood and bone marrow. B cellGRKO mice exhibit impaired IgG response to T-independent (Type II) Ag.
Key Points T-bet–/– mice induce significant IFN- responses after Salmonella infection. Infection of T-bet–/– mice enhances nonprotective Th17/neutrophil responses. iNOS+ granulomas that fail to constrain Salmonella are induced in T-bet–/– mice.
Key Points N-glycan branching is required for generation of mature B cells. N-glycan branching inhibits development of pre-, immature, and T2 B cells. N-glycan branching promotes CD19 surface expression to inhibit death by neglect.
Key Points Immunity to chronic filarial worm infection is apparent in IL-4Rα–deficient mice. Delayed immunity in IL-4Rα–/– mice is due to suboptimal tissue eosinophilia. Eosinophil recruitment in the absence of IL-4R signaling requires CCR3 and IL-5.
Key Points Chinese alligator has a complicated genomic organization of the TCRα/ locus. Unidirectional transfer of V from IgH to TCR locus occurred frequently in vertebrate. A model explaining the evolutionary pattern of atypical VH genes was proposed.
Key Points P2X5 is required for early protective immunity to L. monocytogenes. Macrophages use P2X5 for L. monocytogenes–induced inflammasome activation and L. monocytogenes killing. P2X5-dependent anti–L. monocytogenes functions are independent of both P2X7 and extracellular ATP.
Key Points Neutralizing mAb 2–12C reduces influenza viral load and lung pathology in pigs. DNA plasmid–encoded 2–12C reduces lung pathology. The pig is a useful preclinical model for testing mAbs and mAb delivery platforms.
Key Points GH reprograms inflammatory macrophages to an anti-inflammatory phenotype. GH modulates inflammation by altering activin A secretion and MAFB-dependent genes.
Key Points Targeting different receptors on cDC1s impacts immune responses. Targeting Xcr1 induces Th1 polarization in vivo and in vitro. Targeting hemagglutinin to Xcr1 or Clec9A induces protection from influenza challenge.
Key Points Dexamethasone impairs NK cell cytotoxicity by suppressing LIMK F-actin regulation. Lipoxin A4 induces LIMK to promote lytic granule trafficking and NK cell killing.
Key Points Pulmonary IL-25 expression is induced in response to C. neoformans infection. IL-25 signaling supports fungal dissemination by promoting type 2 immune response. Th2 cells are responsible for IL-25–mediated cryptococcal dissemination.
Key Points PU.1 and IRF4 are required for PD-L2 expression in dendritic cells. PU.1 and IRF4 transactivate the Pdcd1lg2 gene via direct binding to an EICE sequence. PU.1 is involved in the p300-mediated histone acetylation of the Pdcd1lg2 gene.
Key Points T cells produce IL-17A after cryptococcal infection. IL-17A regulates Th1-mediated protection against cryptococcal infection. Tg mice highly expressing TCR specific for cryptococcal Ag were generated.
Key Points Impaired TFH/IgA axis in ATF3-deficient mice leads to dysbiosis of gut microbiota. Dysbiosis of gut microbiota aggravates colitis in the absence of ATF3.
Key Points TCR affinity is associated with CTL ability to kill reactivated HIV-infected cells. Ag sensitivity correlates with CTL killing capacity. Clonal selection of high-affinity clonotypes may contribute to HIV control.
Key Points High-dimensional single-cell analysis uncovers heterogeneity in flow cytometry data. Correct data transformation of flow cytometry data is crucial for interpretation. Extensively documented R code incorporates existing single-cell analysis tools.
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