Explore the vast range of titles available.

Small secondary metabolites, including glucosinolates and the major phytoalexin camalexin, play important roles in immunity in Arabidopsis thaliana. We isolated an Arabidopsis mutant with increased resistance to the powdery mildew fungus Golovinomyces cichoracearum and identified a mutation in the gene encoding cytochrome P450 83A1 monooxygenase (CYP83A1), which functions in glucosinolate biosynthesis. The cyp83a1-3 mutant exhibited enhanced defense responses to G. cichoracearum and double mutant analysis showed that this enhanced resistance requires NPR1, EDS1, and PAD4, but not SID2 or EDS5. In cyp83a1-3 mutants, the expression of genes related to camalexin synthesis increased upon G. cichoracearum infection. Significantly, the cyp83a1-3 mutant also accumulated higher levels of camalexin. Decreasing camalexin levels by mutation of the camalexin synthetase gene PAD3 or the camalexin synthesis regulator AtWRKY33 compromised the powdery mildew resistance in these mutants. Consistent with these observations, overexpression of PAD3 increased camalexin levels and enhanced resistance to G. cichoracearum. Taken together, our data indicate that accumulation of higher levels of camalexin contributes to increased resistance to powdery mildew.

STAT2 is a transcription factor activated by type I and III IFNs. We report 23 patients with loss-of-function variants causing autosomal recessive (AR) complete STAT2 deficiency. Both cells transfected with mutant STAT2 alleles and the patients' cells displayed impaired expression of IFN-stimulated genes and impaired control of in vitro viral infections. Clinical manifestations from early childhood onward included severe adverse reaction to live attenuated viral vaccines (LAV) and severe viral infections, particularly critical influenza pneumonia, critical COVID-19 pneumonia, and herpes simplex virus type 1 (HSV-1) encephalitis. The patients displayed various types of hyperinflammation, often triggered by viral infection or after LAV administration, which probably attested to unresolved viral infection in the absence of STAT2-dependent types I and III IFN immunity. Transcriptomic analysis revealed that circulating monocytes, neutrophils, and CD8+ memory T cells contributed to this inflammation. Several patients died from viral infection or heart failure during a febrile illness with no identified etiology. Notably, the highest mortality occurred during early childhood. These findings show that AR complete STAT2 deficiency underlay severe viral diseases and substantially impacts survival.

Background: Children, including the estimated 7% with food allergy, spend most of their waking hours in school. Variations in school-based food allergy (FA) practices exist. We aimed to examine differences in FA management practices across schools in Canada and the United States (US). Methods: Parents of children with Immunoglobulin E (IgE)-mediated FA were recruited through social media to complete a survey evaluating the schools’ stock epinephrine, epinephrine storage locations, school type, and location. Data were described, analyzed using logistic and linear regressions, and then reported as odds ratios (ORs) and standardized coefficients (b), respectively, with corresponding 95% confidence intervals (95%CIs) and p < 0.05. This study was approved by the University of Manitoba Health Research Ethics Board. Results: Overall, 177 participants (14% [26/177] Canada, 86% [151/177] US) were included. Children were, on average, 4.92 ± 3.12 years and were commonly but not mutually exclusively allergic to tree nuts (50% Canada; 40% US) and peanuts (33% Canada; 29% US). Compared to US parents, Canadian parents were more likely to report epinephrine self-carriage by their children (OR = 4.58; 95%CI = 1.67–12.59). Parents with children age > 5 years were more likely to report epinephrine self-carriage by their children (OR = 3.70; 95%CI = 1.38–9.93) but less likely to report that their children’s school had an allergen-friendly zone (OR = 0.25; 95%CI = 0.06–0.99). Compared to US parents, Canadian parents were more likely to report their child’s school had anaphylaxis management policies (OR = 8.98; 95%CI = 1.11–72.42). Conclusions: Significant in-school FA management differences exist between countries. These findings stress the need for consistent policies and practices to ensure effective care.

This cross-sectional study examines households that exclude allergens by specific food allergy and the association of food allergy-related psychosocial functioning.

Background: Children spend the majority of their waking hours in school. An estimated 20% of all food-triggered anaphylaxis (the most severe food allergic reactions) occur in schools. Although food allergy does not discriminate by socio-economic status, ethnicity or country of residence, school-based food allergy policies vary widely, thereby potentially putting students with food allergy at risk for severe allergic reactions. Aim: We aim to report on the creation of a parent-reported questionnaire on food allergy management in Canadian and American schools. Summary: Informed by content experts and a review of existing questionnaires, and guided by current recommendations on ethnicity, diversity and inclusion, we developed a questionnaire intended to provide insight into school-based food allergy management, across two countries, and using language that is respectful and reading levelappropriate for diverse populations. In particular, we focused on suitability for populations from diverse socio-economic status and ethnicity, while accounting for socio-political differences between Canada and the United States. Efforts to ensure that we have developed a survey that meets our diversity goals include engagement with school principals and parents of children with food allergy. Discussion: Our questionnaire will amplify voices of diverse populations affected by food allergy, with the goal of enhancing food allergy management practices in schools. Such understanding is critical for nutrition professionals who work with schools to develop food programs, and for the development of patient education materials that also respect these diversity goals.

STAT2 is a transcription factor activated by type I and III IFNs. We report 23 patients with loss-of-function variants causing autosomal recessive (AR) complete STAT2 deficiency. Both cells transfected with mutant STAT2 alleles and the patients' cells displayed impaired expression of IFN-stimulated genes and impaired control of in vitro viral infections. Clinical manifestations from early childhood onward included severe adverse reaction to live attenuated viral vaccines (LAV) and severe viral infections, particularly critical influenza pneumonia, critical COVID-19 pneumonia, and herpes simplex virus type 1 (HSV-1) encephalitis. The patients displayed various types of hyperinflammation, often triggered by viral infection or after LAV administration, which probably attested to unresolved viral infection in the absence of STAT2-dependent types I and III IFN immunity. Transcriptomic analysis revealed that circulating monocytes, neutrophils, and CD8+ memory T cells contributed to this inflammation. Several patients died from viral infection or heart failure during a febrile illness with no identified etiology. Notably, the highest mortality occurred during early childhood. These findings show that AR complete STAT2 deficiency underlay severe viral diseases and substantially impacts survival.