This dataset provides a longitudinal analysis of urinary metabolomic profiles from 198 children aged 1 month, 6 months, 1 year, 3 years, and 5 years. Demographic information, including birth history, feeding practices, parental atopic history, household income, and atopic disease status at different ages, was collected. Total and allergen-specific IgE levels (mite, egg, cow's milk) were measured to evaluate allergic sensitization over time. Atopic disease status was also monitored at multiple time points to assess its development. The urinary metabolomic data, generated using advanced 1H-nuclear magnetic resonance (NMR) spectroscopy, were processed and normalized to support robust metabolic modeling. This dataset aims to provide insights into the relationships among early growth, metabolomic changes, and the development of allergic sensitization and atopic diseases in early childhood.

Oral co-exposure to Clostridioides difficile toxin A and ovalbumin disrupts intestinal homeostasis and predisposes to food allergy in mice.

Food allergies are increasing worldwide, yet the early epithelial mechanisms that initiate allergic sensitization remain incompletely defined. As the intestinal epithelium governs both allergen translocation and epithelial–immune crosstalk, it constitutes a critical but underutilized model for predicting allergenicity. In this study, we used Caco-2 and T84 intestinal epithelial monolayers cultured on Transwell® inserts to compare barrier properties and responses to peanut protein extract. Phenotypic characterization included biomarker profiling, transepithelial electrical resistance (TEER) measurements, tight junction integrity assessment, and analysis of cytokine levels as well as oxidative and nitrosative stress. Peanut exposure caused moderate TEER reductions without overt tight junction disruption while allowing translocation of the major allergen, Arachis hypogaea allergen 1 (Ara h 1), likely via transcellular pathways. Peanut protein extracts also induced epithelial stress responses, characterized by increased reactive oxygen species and nitric oxide production, alongside time-dependent secretion of innate and type 2-associated mediators, including IL-1β, TSLP, IL-25, and IL-33, indicating epithelial activation in the absence of complete barrier breakdown. Notably, basolateral supernatants from peanut-exposed epithelial monolayers activated THP-1-derived macrophages and enhanced IL-6 secretion, demonstrating that limited allergen passage across an otherwise intact epithelial barrier is sufficient to elicit early innate immune responses. Collectively, these findings indicate that peanut extract induce subtle functional perturbations in the intestinal epithelium while promoting downstream immune activation, highlighting Caco-2 and T84 cells as complementary in vitro platforms for studying barrier-dependent mechanisms of allergic sensitization.

Background Gel manicure is widely used in professional and home settings. Concerns relate to chemical exposure from acrylate containing nail products, ultraviolet radiation emitted by nail curing lamps, occupational exposure among nail technicians, and potential microbiological implications. Aims To systematize published evidence on health effects associated with gel manicure use, with emphasis on allergic reactions, ultraviolet exposure related outcomes, occupational risks, and microbiological findings, and to identify gaps in the current evidence base. Methods A narrative review was conducted using PubMed, Google Scholar, and ResearchGate. Publications from January 2010 to March 2025 were considered. Only English language articles were included. Inclusion criteria comprised randomized controlled trials, cohort studies, case control studies, systematic reviews, meta analyses, and international or national guidelines reporting health effects or exposure characteristics related to gel manicure use. Exclusion criteria included single case reports, conference abstracts, non peer reviewed publications, animal studies, and articles lacking explicit data on gel manicure exposure or associated health outcomes. The initial search yielded 223 records, and 44 publications were retained for analysis. Results Nail curing devices predominantly emit UVA radiation with peak wavelengths between 365 and 405 nm, with substantial variability across lamp types and designs. Under typical usage conditions, cumulative ultraviolet exposure during manicure sessions remains below levels associated with clinically significant dermatologic damage or increased skin cancer risk. Allergic contact dermatitis related to acrylate and methacrylate containing products is the most frequently reported adverse outcome, particularly among nail technicians and younger users. Evidence on microbial retention and reduced hand hygiene effectiveness with gel or artificial nails is heterogeneous and context dependent. Conclusions Available evidence indicates that allergic sensitization to acrylate containing nail products represents the primary clinically relevant health risk of gel manicure, whereas ultraviolet radiation related carcinogenic risk appears minimal under typical use. Standardization of exposure assessment and further research on occupational and microbiological outcomes are needed.

The substantial increase in food allergy prevalence during the last decades has made it a significant public health concern, affecting around 10% of the global population, especially children. Despite significant progress in understanding the general mechanisms of allergic sensitization, the development of oral tolerance remains a major challenge in advancing food allergy research and treatment. Additionally, each allergenic food source has a distinct immunological profile and tolerance trajectory, further complicating research efforts. Currently, oral allergen-specific immunotherapy is the only treatment that can help build tolerance to certain food allergens over time-although treatment outcomes vary. While B cells have been described and studied for their pathogenic role in food allergy, recent evidence suggests that they also modulate allergic responses through various effector and humoral functions. Notably, despite their low frequency, recent knowledge on the molecular and functional characteristics of food allergen-specific memory B cells has revealed important functions during both disease progression and therapeutic intervention. This review summarizes the current knowledge of IgE-mediated food allergy, highlighting the role of B cells, especially allergen-specific ones, in both disease and immune tolerance.

Exposomic determinants substantially influence the variability of molecular IgE-mediated sensitization in allergic rhinitis and conjunctivitis across bioclimatic regions, underscoring their relevance in precision allergology. This study aimed to characterize molecular sensitization profiles in Spanish patients with respiratory allergy from distinct geographic and climatic areas. A cross-sectional, multicenter study was performed in 12 Spanish cities. The study population comprised 291 patients diagnosed with allergic rhinitis and/or conjunctivitis according to the modified ARIA/DECA criteria. Participants underwent skin prick testing with standardized allergen extracts and multiplex molecular IgE analysis. Clinical, demographic, and regional bioclimatic variables were integrated to define exposomic sensitization patterns. Patients previously treated with allergen immunotherapy or biologics were excluded. Regional pooled sera were analyzed by ELISA and IgE immunoblotting to validate molecular data and identify IgE binding to nonrecombinant or poorly characterized allergenic components. Distinct regional sensitization profiles were identified. Grass pollen allergens predominated in oceanic and continental climates, while olive and cypress pollens were more frequent in Mediterranean areas. Sensitization to house dust mite, particularly Dermatophagoides pteronyssinus and Blomia tropicalis, was highly prevalent in subtropical and humid zones. Molecular assays confirmed skin test findings and identified major allergenic molecules, including Phl p 1, Ole e 1, Der p 1, and Der p 2, along with region-specific components such as Der p 23, Cup a 1, Alt a 1, and Pla a 2. This multicenter exposomic study demonstrated that climatic diversity modulates allergen sensitization in Spain, supporting region-tailored precision diagnostic and therapeutic strategies in respiratory allergy.

Background/Objectives: Food allergy (FA) is a substantial health burden in children. FA is often associated with malnutrition and malabsorption, due to restrictive food avoidance diets, which can significantly impair the patient's and their family's quality of life. To this date, population-based data combining sensitization and clinical allergy remain limited. This study aimed to assess the patterns of sensitization rates to food and food allergy prevalence rates in Croatian children and to evaluate differences according to age, sex, and region of origin. Materials and Methods: In this cross-sectional study, 1948 preschool and school-aged children from three Croatian regions (Zagreb, Dalmatia, and Slavonia) were included. Participants underwent skin prick testing to common food and inhalant allergens. Data on personal and family medical history were collected using questionnaires and medical records. FA prevalence was evaluated using self-reported data in school-aged children and physician-diagnosed FA data in preschool children. Results: Overall, 41% of participants were sensitized to at least one allergen, while 13% were sensitized to at least one food allergen. Tree nuts-particularly hazelnut-were the most common food-derived sensitizers, followed by hen's egg, cow's milk, and fish. Boys exhibited higher total sensitization rates than girls (44.2% vs. 37.5%; p = 0.001), higher food allergen sensitization rates (14.7% vs. 11.4%; p = 0.037), and higher total polysensitization rates (30.7% vs. 22.6%; p < 0.001). School-aged children showed higher total sensitization (44.8% vs. 33.4%; p < 0.001) and polysensitization rates (29.8% vs. 20.5%; p < 0.001) than preschool children, while sensitization to food allergens did not differ between age groups. Food allergen sensitization rates differed by region, with higher prevalence in Zagreb compared with Dalmatia and Slavonia (p = 0.0055), whereas total sensitization rates did not differ regionally. The agreement between sensitization and self-reported FA among school-aged children was low (κ = 0.22; p < 0.001), as was the agreement between sensitization and physician-diagnosed FA in preschool children (κ = 0.13; p < 0.001), despite high specificity in both analyses (95% and 99%%, respectively). Conclusions: Allergic sensitization is common among Croatian children, but it poorly predicts clinically relevant food allergy. These findings highlight the multifactorial nature of allergen sensitization in children and emphasize the need for improvements in diagnostic pathways, targeted prevention strategies, and continued surveillance to optimize allergy prevention and management in children.

Food allergy is an increasing global health burden, particularly in industrialized countries, with rising prevalence in both pediatric and adult populations. It is characterized by exaggerated immune responses to innocuous dietary antigens, leading to clinical manifestations ranging from mild gastrointestinal symptoms to life-threatening anaphylaxis. Mast cells are central effectors in the pathophysiology of food allergy, initiating and amplifying allergic inflammation through the release of a broad array of mediators upon activation. Recent studies have revealed that the intestinal microbiota plays a critical role in shaping immune responses, including the regulation of mast cell development, maturation, and activation. Moreover, dysbiosis has been associated with increased susceptibility to allergic sensitization and heightened mast cell reactivity. This review explores the molecular mechanisms underlying the microbiota-mast cell axis in the context of intestinal homeostasis and food allergy with a particular emphasis on the regulation of mast cell effector functions by TLR signaling and microbial metabolites. We also discuss the therapeutic potential of targeting the microbiota-mast cell axis as novel strategies to restore immune tolerance. Understanding this complex crosstalk opens new avenues for translational approaches in the prevention and treatment of food allergy.

This study aimed to analyze allergen profiles associated with respiratory allergic diseases in pediatric populations in Guangzhou, China, and provide a theoretical basis for prevention and management strategies. A cross-sectional study was conducted among 1,230 children between 0 and 14 years of age who underwent allergen-specific immunoglobulin E antibody testing via immunoblotting at a hospital in Guangzhou, Guangdong Province, China, between January 2020 and January 2024. Positivity rates for allergens were analyzed and compared across categories (type and grade), age groups, seasons, and sex. Sensitization to at least one allergen was detected in 43.9% (n = 540) of the children. The overall sensitization rate did not differ significantly by sex or among age groups (p > 0.05). The predominant inhalant allergen was Dermatophagoides farinae / Dermatophagoides pteronyssinus (22.93%, n = 282), while the most common food allergen was egg white / egg yolk (10.73%, n = 132) (p < 0.05). Allergen positivity ranged from one to five allergen types, with frequency decreasing as the number of allergens increased (p < 0.05). A shift in the dominant allergen type was observed with increasing age: food allergens were common among infants and toddlers (p < 0.05), whereas inhalant allergens were dominant among preschool and school-age children (p < 0.05). The allergen sensitization spectrum among children with respiratory allergies in Guangzhou exhibits a distinct pattern that evolves with age. The predominant allergens among infants and toddlers were food-based, specifically milk, beef / lamb, and egg white / egg yolk, whereas among preschool and school-age children, inhalant allergies, particularly Dermatophagoides farinae / Dermatophagoides pteronyssinus and house dust, were most prevalent. These region-specific findings highlight the importance of implementing age-appropriate strategies for the diagnosis, prevention, and management of pediatric respiratory allergic diseases.

Atopic dermatitis is a chronic inflammatory skin condition marked by intense itching and a weakened skin barrier. The compromised skin barrier often leads to exaggerated immune responses and greater sensitivity to allergens. Previous studies have already implicated a link between obesity and atopic dermatitis; however, the mechanisms linking obesity to atopy are not yet well understood. We propose that obesity impairs skin barrier function, facilitating allergen penetration in the skin and triggering systemic and local allergic sensitization. We used a diet-induced obesity mouse model to examine skin barrier integrity and immune responses in both steady-state and inflammatory conditions. In order to induce dermatitis or food allergy, we epicutaneously applied MC903 or ovalbumin, respectively. We observed that obesity significantly alters skin barrier physiology, as indicated by increased transepidermal water loss in obese animals. Over time, we observed a decrease in key skin barrier proteins-preceding overt cutaneous inflammation, further indicating a loss of barrier integrity during obesity. Interestingly, skin barrier breakdown was independent of changes to the microbiome. On a cellular level, immune profiling revealed a shift towards a type 17 helper T-cell response bias, although this shift did not coincide with an increase in cytokine production under steady-state conditions. Topical application of MC903 in obese animals led to increased ear swelling and a pronounced Th17-biased inflammatory response compared to lean counterparts. Our findings show that obesity weakens the skin barrier, facilitating increased allergen penetration and allergic sensitization. The Th17-skewed immune environment in obese animals may also amplify inflammatory responses to allergens and act as a feed-forward loop to further disintegrate the skin barrier. This study highlights how obesity-induced skin barrier dysfunction contributes to allergic conditions like atopic dermatitis and may be therapeutically targeted by barrier restoration.

Epicutaneous application of house dust mite induces allergic skin inflammation and atopic march to the lung upon airway allergen challenge.

Eosinophilic esophagitis (EoE) is an immune-mediated disease characterised by oesophageal eosinophilic infiltration, leading to chronic inflammation and tissue remodelling. To describe the clinical, epidemiological and endoscopic characteristics of children with EoE in Colombia, and explore associations between symptoms, allergen sensitisation and endoscopic findings. Observational, multicentre retrospective study with an analytical component, conducted on paediatric patients diagnosed with EoE across 10 tertiary referral centres in Colombia between 2015 and 2023. All cases had histological confirmation with ≥15 eosinophils per high-power field. Data were extracted from standardised medical records by trained investigators. A total of 143 cases were included, with a male predominance (66.4%) and median age at diagnosis of 92 months (IQR 56-144). Relevant early exposures included prematurity (11.2%), low birth weight (10.5%), caesarean delivery (50.3%), infant formula use (62.2%) and antibiotics in infancy (27.9%). Family history of atopy was present in 54.6%, and EoE in 4.9%. Food specific IgE was present, particularly to cow's milk (56.6%) and egg (38.1%). Most frequent symptoms included abdominal pain (67.1%), nausea (60.1%) and vomiting (46.2%). Endoscopic findings included longitudinal furrows (70.9%) and white exudates (67.4%). Statistically significant associations were found between dysphagia and oesophageal rings (p=0.003), vomiting and white exudates (p=0.018), abdominal pain and longitudinal furrows (p=0.025) and regurgitation and oedema (p=0.031). Paediatric EoE in Colombia shows symptom and endoscopic heterogeneity. Identifying potential allergen triggers may contribute to understanding symptoms and endoscopic patterns in EoE.

Sensory neurons promote allergic sensitization and cross-sensitization via mTORC1.

Allergic diseases are caused by overexuberant type II immune responses mounted against environmental antigens1. The allergic state is typified by the presence of allergen-reactive immunoglobulin E (IgE), which triggers mast cell degranulation upon allergen encounter, manifesting in pruritis, oedema and, in severe cases, anaphylaxis. Over the past century, the prevalence of allergic diseases has increased markedly, suggesting that environmental rather than genetic factors are mediating this change2. Although many hypotheses connecting environment to allergy exist3-6, the biological mechanisms that underpin environmentally mediated protection from allergy are unknown. Here we show, using a mouse model of allergic disease, that exposure to immunostimulatory environments generated cross-reactive adaptive immune memory, which tracked with obstructed type II immune responses upon allergen exposure. We found that engagement of cross-reactive adaptive immunity protected against future allergic sensitization and suppressed established allergic responses. Cross-reactivity in a tolerogenic context also prevented allergy, with the effect extending across antigenically complex exposures even at low protein sequence similarity. Our findings demonstrate a mechanistic relationship between environment and allergy, with general implications for adaptive immune function in natural settings.

Introduction. Identifying the causes of allergic diseases and allergen sensitization patterns in young children remains a challen­ ging task of significant interest to the medical community. Objective. This study aimed to determine risk factors, sensitization profiles, and major allergens in children aged 2–4 years with allergic rhinitis (AR) residing in Beloretsk (Republic of Bashkortostan). Materials and methods. In this open-label, single-center, prospective study, 113 children with persistent rhinitis were enrolled and divided into two groups: AR (n = 68, mean age 3.19±0.78 years) and non-AR (n = 45, 3.00±0.80 years). Evaluations included medical history, eosinophilic cationic protein levels, total and specific IgE (ImmunoCAP), and nasal cytology. Polysensitized children (n = 11) underwent further testing using the ISAC-112 molecular panel. Statistical analysis employed median (Me) with 95% confidence intervals (95% CI), Mann — Whitney U-test, Yates-corrected χ ² test, Spearman’s correlation coefficient, and Chaddock’s scale. Results. AR developed by the age of three, with 54.41% of patients exhibiting mild persistent perennial symptoms (p = 0.019), predominantly sneezing (p &lt; 0.001). Significant risk factors included family history of asthma (OR 11.9; 95% CI [2.8; 50.9]), seasonal AR (OR 2.5; 95% CI [1.1; 5.7]), maternal anemia (OR 2.3; 95% CI [1.1; 5.0]), cesarean delivery (OR 2.8; 95% CI [1.2; 6.8]), atopic dermatitis (OR 3.9; 95% CI [1.4; 10.3]), adenoid hypertrophy grade 2—3 (OR 3.2; 95% CI [1.3; 8.1]), animal exposure (OR 3.6; 95% CI [1.8; 7.3]), and passive smoking (OR 2.8; 95% CI [1.4; 5.8]). Sensitization was detected to cat dander (75.00%), dog dander (66.18%), birch (47.06%), timothy grass (20.59%), mugwort (36.76%), and house dust mites (D. p., D. f.) (41.18%). Molecular analysis (ISAC-112) confirmed sensitization to Fel d 1 (90.91%) and Bet v 1 (73.72%). Conclusion. These findings highlight the importance of regional studies in understanding the clinical and risk factors of pediatric allergic diseases, contributing to improved diagnosis and prevention strategies.

Allergic diseases are on the rise worldwide, driven by respiratory epithelial barrier dysfunction that promotes sensitization to inhalant allergens such as pollen, dust mites, pet dander, and fungal spores. These antigens trigger IgE-mediated immune responses that lead to diseases such as allergic rhinitis (AR) and asthma. B cells play a central role by producing allergen-specific IgE, presenting antigens, releasing cytokines, and forming memory B cells (MBCs). Their differentiation into IgE-secreting plasma cells (PCs) mainly relies on T cell help, germinal center (GC) reactions, and/or extrafollicular responses and class switch recombination (CSR), which makes them important therapeutic targets. The nasal mucosa, as the first point of contact for allergens, acts both as a barrier and as an immunological site. In AR, IL-13-driven goblet cell hyperplasia and overproduction of mucus compromise the integrity of the barrier. Although the nasal microbiome can influence the immune response, its role in atopy remains unclear. Local B cell activity, including extrafollicular IgE production and ectopic GCs, enhances mucosal immunity. Epithelial cells detect allergens via pattern recognition receptors (PRRs) and release alarmins (IL-25, IL-33, TSLP), which can trigger type 2 inflammation. Proteases from allergens such as house dust mites (HDM) disrupt epithelial junctions, while pollutants, smoke, microplastics, and allergen-derived metabolites further modulate immune activation. Allergens are transported to the lymph nodes by the passive flow to follicular dendritic cells (FDCs) or by active uptake by interferon regulatory factor (IRF) 4-dependent conventional type 2 DCs, which activate T follicular helper (TFH) cells to drive IgE responses. Advanced lymphoid organoids that mimic the microenvironment of GCs offer promising models for the study of allergic sensitization but require improved standardization.

Food allergies represent a growing global public health challenge arising from complex interactions among genetic predisposition, environmental exposures, dietary habits, and gut microbiota. Sensitization may occur through dermal, respiratory, or gastrointestinal routes and is strongly influenced by epithelial barrier dysfunction and Th2-skewed immune responses. A detailed understanding of allergen structure, immune recognition, and sensitization pathways is therefore essential for the development of effective mitigation strategies. Both thermal and non-thermal food processing technologies have been investigated for their ability to reduce the allergenicity of common foods, including milk, egg, peanut, tree nuts, and seafood. Conventional thermal processing can denature allergenic proteins and enhance digestibility, but may also adversely affect nutritional value and sensory quality. In contrast, emerging non-thermal technologies—such as High Hydrostatic Pressure (HHP), Pulsed Ultraviolet (PUV) light, cold plasma, ultrasound, pulsed electric fields, and gamma irradiation—offer alternative approaches that induce targeted structural modifications in allergenic proteins while better preserving product quality. However, the effectiveness of these technologies is highly context-dependent, varying with the food matrix, processing parameters, and allergen type; moreover, reductions in Immunoglobulin E (IgE) reactivity observed in vitro do not always translate into clinically meaningful outcomes. Limitations in standardized allergenicity assessment, insufficient in vivo and clinical validation, and challenges related to scalability and regulatory acceptance remain significant barriers. This review integrates immunological mechanisms with food engineering perspectives to critically evaluate thermal and non-thermal processing strategies, highlighting the translational potential of non-thermal technologies as promising, scalable tools for developing safe, quality-preserving, and clinically relevant hypoallergenic foods.

Atopic allergy is rising globally and placing a significant strain on healthcare systems, yet the understanding of the underpinning mechanisms of allergic sensitization remains incomplete. Extracellular vesicles (EVs) have recently emerged as important mediators of immune modulation, due to their diverse cargo, and therefore may play a mechanistic role in allergic sensitization development. Thus, this study investigated whether EVs released by activated dendritic cells (DCs) contribute to allergic sensitization of the common egg allergen, ovalbumin (OVA). DCs were generated from human monocytes cultured with GM-CSF and IL-4, then stimulated with LPS and/or OVA. EVs were subsequently isolated using size-exclusion chromatography and added to freshly isolated naive T cells at defined time points. T cell responses were then analyzed using spectral flow cytometry. The results highlight that EVs derived from LPS or LPS + OVA-stimulated DCs enhanced IL-4 production and reduced IFN-γ production in naive T cells from egg-allergic donors, indicating a shift toward a Th2 profile. In healthy donors, LPS-induced DC EVs also suppressed IFN-γ expression. Notably, EVs alone were insufficient to activate T cells without CD3/CD28 co-stimulation, suggesting that EVs may function as a "third signal" shaping T cell polarization. These findings highlight a potential role for DC-derived EVs in initiating allergic sensitization.

BackgroundThe use of molecular allergens have greatly improved the clinical relevance of specific IgE serologies during allergy work-up. Very little is known regarding the added value of molecular allergens in the results of the basophil activation test (BAT).ObjectiveTo study the BAT concordance when using similar amounts of molecular allergens against source extracts, and to assess factors associated with BAT discrepancies between extract and related component.MethodsSystematic retrospective monocentric study of all BAT performed at the Trousseau Hospital, Paris, France, with both molecular components and corresponding extract.ResultsData from 213 interpretable extract/component BAT pairs (89 cow milk, 70 wheat, 28 house dust mites (HDM), 12 peanut, 9 hen egg, 3 peach, 1 apple, 1 chicken meat), corresponding to 150 blood samples from 109 patients were analyzed. Among BAT pairs showing allergen sensitizations, the two reagents only showed moderate agreement (κ = 0.62), with 18% (36/201) discordant BAT results. Among 36 cases of discrepant BAT results between extract and molecular component, 69% (25/36) were extract+/component– (p=0.03), in line with genuine allergic status, in contrast with the opposite case. Even in extract+/component+ concordant cases, component-stimulated basophils showed 6% less activation rates than their extract-stimulated counterpart. After stratification by allergen, better performances were confirmed with cow milk extract, but not with other allergens, which display large disparity regarding the propensity of different molecular component to activate basophils. Independently of the considered allergen, other variables such as total IgE, BAT positive control values, and treatment with monoclonal antibody or allergen-specific immunotherapy, appear to further modulate the risk of presenting a discordant BAT result.ConclusionIn our study population, molecular components had lower capacity than the corresponding extract to activate IgE-sensitized basophils, which partly explain higher rates of true positive extract+/component– BAT. Component-based BAT can potentially lead to false-negative results, and extract-based should generally be preferred, especially for cow milk.

So far, knowledge of determinants of the presence of systemic autoantibodies (AABs) in the population is limited. Here, we investigated possible associations between serum AABs and allergies, using data on allergic sensitization and diagnoses of allergic diseases. In 331 participants of a population-based study, 5 humoral systemic AABs and 7 AAB screening tests were analyzed. Allergic sensitization was characterized by specific IgE concentrations in serum samples (CAP class ≥ 2); additionally, self-reported diagnoses of allergic diseases were used as exposure variables. Multivariable adjusted logistic regression models were applied to explore the association with AAB test positivity; all analyses were stratified by sex. In a sensitivity analysis, AAB test results were defined as non-normal and normal. In 46.2% and 37.1% of female and male study participants, respectively, at least one positive AAB test was identified. Allergic sensitization was observed in 23.8% and 29.7% of female and male participants, while 26.2% and 9.3% reported at least one diagnosis of allergic disease, respectively. Positive associations between allergic sensitization and serum AABs were identified in women for rheumatoid factor (RF), antinuclear antibodies (ANA), and at least one positive AAB test; in men, there was some indication for an association with anti-neutrophil cytoplasmic antibody (ANCA) positivity. Self-reported diagnosis of allergic diseases was not significantly associated with the AAB positivity. In this population-based group of adults, there is evidence for an association between allergic sensitization and systemic AABs, almost exclusively in women. Large prospective studies are needed for confirmation and further investigation of individual AABs.