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Hanson, I. C.

Publications and source records attributed to Hanson, I. C..

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Utility of Shrimp and Der p 10 specific IgE for Shrimp Allergy Diagnosis in Non-House Dust Mite Sensitized Patients

BackgroundThere are no set specific IgE (sIgE) to predict shrimp allergy as cross-reactivity with other arthropods play a role in shrimp sensitization.\n\nObjectiveThis study identifies the allergens associated with shrimp allergy in house dust mite (HDM) and non-HDM sensitized patients.\n\nMethodsPatients with shrimp sensitization (positive skin prick test [SPT] and/or sIgE) with/without history of clinical reaction were recruited. Allergy was confirmed by oral food challenge (OFC) except for patients with history of anaphylaxis. Shrimp allergic (SA) and shrimp tolerant (ST) patients were further classified based on HDM sensitivity. The sIgE to shrimp, shrimp and HDM components were performed. Fishers exact test, Wilcoxon sum rank test and receiver operating characteristics analyses were done.\n\nResultsOf 79 patients recruited, 12 SA (7 positive OFC and 5 with history of anaphylaxis), 18 ST and 10 non-shrimp sensitized controls (NC) were enrolled. In non-HDM sensitized patients, sIgE to shrimp (10.5 kUA/L, p=0.012) and Der p 10 (4.09 kUA/L, p=0.035) were higher in SA patients. Shrimp sIgE [≥]3.55 kUA/L had 100% sensitivity and 85.71% specificity (ROC=0.94[0.81, 1.0]). Der p 10 sIgE [≥]3.98 kUA/L had sensitivity of 80% and specificity of 100% (ROC=0.86[0.57, 1.0]). rPen a 1 [≥]1.1 kUA/L had sensitivity of 80% and specificity of 85.7% (ROC=0.80[0.47,1.0]).\n\nConclusionsIn non-HDM sensitized patients, shrimp sIgE [≥]3.55 kUA/L and Der p 10 sIgE[≥]3.98 kUA/L give 100% sensitivity and specificity, respectively, to diagnose shrimp allergy. HDM sensitivity can influence sIgE levels to shrimp and shrimp/HDM components due to cross-reactivity.

immunology

Ruxolitinib partially reverses functional NK cell deficiency in patients with STAT1 gain-of-function mutations

BackgroundNatural Killer (NK) cells are critical innate effector cells whose development is dependent on the JAK-STAT pathway. NK deficiency can result in severe or refractory viral infections. Patients with Signal Transducer and Activator of Transcription (STAT)1 gain of function (GOF) mutations have increased viral susceptibility.\n\nObjectiveWe sought to investigate NK cell function in STAT1 GOF patients. Methods: NK cell phenotype and function were determined in 16 STAT1 GOF patients.\n\nMethodsNK cell phenotype and function were determined in 16 STAT1 GOF patients.NK cell lines expressing patient mutations were generated with CRISPR-Cas9 mediated gene editing. STAT1 GOF NK cells were treated in vitro with ruxolitinib.\n\nResultsPeripheral blood NK cells from of STAT1 GOF patients had impaired terminal maturation. Specifically, patients with STAT1 GOF mutations have immature CD56dim NK cells with decreased expression of CD16, perforin, CD57 and impaired cytolytic function. STAT1 phosphorylation was elevated but STAT5 was aberrantly phosphorylated in response to IL-2 stimulation. Upstream inhibition of STAT signaling with the small molecule JAK1/2 inhibitor ruxolitinib in vitro and in vivo restored perforin expression in CD56dim NK cells and partially restored NK cell cytotoxic function.\n\nConclusionsProperly regulated STAT1 signaling is critical for NK cell maturation and function. Modulation of elevated STAT1 phosphorylation with ruxolitinib is an important option for therapeutic intervention in patients with STAT1 GOF mutations.

immunology