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PubMed1992

The effect of T-cell depletion on enhanced basophil histamine release after in vitro incubation with live influenza A virus.

A number of mechanisms participate in virus-induced asthma. Previously, we described enhanced basophil histamine release (HR) during an experimentally induced rhinovirus infection and after in vitro incubation of peripheral blood mononuclear cells (PBMC) with influenza virus. This study extends our previous observations and examines the effect of influenza A virus on basophil leukotriene C4 (LTC4) release as well as the effect of T-cell depletion on virus-enhanced basophil HR. PBMC were isolated from ragweed-allergic subjects and incubated with live influenza A virus or control medium (allantoic fluid). After incubation with influenza A, ragweed antigen (AgE) stimulated LTC4 and HR were enhanced (P less than 0.05). To further define the role of T cells in virus-enhanced basophil secretion, PBMC were isolated and divided into two aliquots. In one aliquot, T cells were removed by magnetic bead separation of mouse monoclonal anti-CD3-coated lymphocytes. T-cell-depleted and nontreated PBMC suspensions were incubated with influenza A or control medium, collected, and challenged with AgE to release histamine. Basophil HR was enhanced in the virus-treated group of PBMC that had not undergone T-cell depletion. In contrast, virus incubation did not enhance HR in the T-cell-depleted fraction. Finally, preliminary analysis of the supernate from virus-treated leukocytes indicates the presence of interferon-gamma. These findings suggest that T cells, and their cytokine products, play an integral role in the process by which viruses enhance basophil HR.

Adult↗
PubMed2007

Induction of Th2 type immunity in a mouse system reveals a novel immunoregulatory role of basophils.

While production of cytokines such as IL-12 by activated dendritic cells supports development of Th1 type immunity, a source of early IL-4 that is responsible for Th2 immunity is not well understood. We now show that coculture of basophils could promote a robust Th2 differentiation upon stimulation of naive CD4 T cells primarily via IL-4. Th2 promotion by basophils was also observed even when naive CD4 T cells were stimulated in a Th1-promoting condition or when fully differentiated Th1 phenotype effector CD4 T cells were restimulated. IL-4-deficient basophils failed to induce Th2 differentiation but suppressed Th1 differentiation. It was subsequently revealed that the IL-4-deficient basophils must engage cell-to-cell contact to exert the inhibitory effect on Th1 differentiation. Stimulation of naive CD4 T cells within an in vivo environment of increased basophil generation supported development of Th2 type immunity. Taken together, our results suggest that basophils may provide an important link for the development of Th2 immunity.

Animals↗
PubMed2004

Actin cytoskeleton-dependent down-regulation of early IgE-mediated signaling in human basophils.

Two regions of down-regulation of FcepsilonRI [high-affinity immunogloublin E (IgE) receptor] signaling have been localized recently in basophils. An early down-regulatory step is located proximal to syk and appears responsible for a transient syk phosphorylation in antigen-stimulated basophils. A second, more distal region appears responsible for the transient activation of the ras-extracellular-regulated kinase (Erk) pathway when syk phosphorylation is sustained in anti-IgE-stimulated basophils. As the actin cytoskeleton has been demonstrated to inhibit the early FcepsilonRI signaling in rat basophilic leukemia cells, we explored the hypothesis that the actin cytoskeleton was responsible for the transience of syk phosphorylation in antigen-stimulated basophils. The inhibition of F-actin polymerization with latrunculin A induced a sustained syk phosphorylation in basophils stimulated with an optimal dose of the antigen benzyl penicilloyl-human serum albumin. However, in the presence of latrunculin A, Erk phosphorylation remained transient after stimulation with the antigen or anti-IgE. Latrunculin A also increased downstream events such as histamine release, leukotriene C(4) release, and the intracellular calcium signal, although some of these effects were not specific for an immunologic stimulus. Our results suggest that the actin cytoskeleton is responsible for down-regulation of FcepsilonRI signaling at a point located proximal to syk phosphorylation. Moreover, the fact that latrunculin A did not result in sustained Erk phosphorylation supports the presence of a second down-regulatory step between syk and Erk that cannot be overcome by a sustained early signal.

Actins↗
PubMed2003

Influence of UVB, UVA and UVA1 irradiation on histamine release from human basophils and mast cells in vitro in the presence and absence of antioxidants.

UV irradiation is widely used for the treatment of atopic eczema. In recent years, UVA1 phototherapy has gained increasing attention. This study analyzed the influence of different UV wavelengths--especially UVA1--on histamine release from human basophils and mast cells. The modulation of this parameter might be responsible for some of the therapeutic effects of UV irradiation. Enriched human basophils and human mast cells (HMC1 cell line) were irradiated with increasing doses of UVB, UVA and UVA1 in vitro. After irradiation, different stimulants were added to induce histamine release. In additional experiments, basophils were preincubated with superoxide dismutase, ascorbate or trolox to study the role of antioxidants in the modulation of histamine release after UV irradiation. UVA and UVA1 significantly inhibited histamine release from basophils and mast cells. UVB only had an inhibitory effect on mast cells. Preincubation with superoxide dismutase and ascorbate did not influence the inhibitory effect of UVA1 on basophil histamine release, whereas trolox decreased significantly the histamine release from nonirradiated basophils.

Adult↗
PubMed1993

Formation of Charcot-Leyden crystals by human basophils in sputum and peripheral blood.

To confirm the formation of Charcot-Leyden crystals (CLC) in basophils, we observed basophils in sputum and peripheral blood. Sealed slide and suspension culture methods were used to observe the process of CLC formation in peripheral blood basophils and eosinophils under electron microscopy. CLC formation was observed in basophils and eosinophils, and was found to be augmented by sealed slide method. A temperature of 4 degrees C was better than 37 degrees C for promoting the formation of crystals. There was no correlation between the degranulation of these cells and the formation of CLC after stimulation with anti-IgE or anti-IgG antibodies. CLC were initially detected in the cytoplasmic granules of basophils where they continued to enlarge. No CLC were identified in mast cells under any conditions studied. These findings confirm that CLC in sputum are not exclusive to eosinophils and that CLC appear to be present in basophil-rich sites under the cell damage.

Asthma↗
PubMed2003

Hemopoietic cells with features of the mast cell and basophil lineages and their potential role in allergy.

Human mast cells (MCs) and basophils play a key role in the pathogenesis of allergic disorders, not only by producing inflammatory and fibrogenic mediators, but also by directly and indirectly secreting various cytokines and chemokines. Although mast cells and basophils have differences in many properties, recent evidence suggests that human MCs and basophils may be derived from a common progenitor, and their contents and phenotypes may be reversibly altered in a variety of allergic disorders. The study of FcetaRI signalling of mast cell and basophils offers new opportunities for therapeutic interventions based on the specific inhibition of the earliest events in allergic diseases. This article reviews the origin, differentiation, morphology and phenotypic properties of MCs and basophils, focussing particularly on the possible pathogenic role of MCs and basophils in allergy and biochemical targets for therapeutic interventions in allergic diseases.

Animals↗
PubMed1996

Airway basophil and mast cell density in patients with bronchial asthma: relationship to bronchial hyperresponsiveness.

We investigated the role of basophils and mast cells in the pathogenesis of bronchial asthma. Eight asthmatics (6 atopic, 2 nonatopic) and 6 control subjects were enrolled in this study. Bronchial responsiveness to acetylcholine (PC20ACh) was measured in asthmatics and endobronchial biopsy from right upper lobe bronchus was performed on the same day. Basophils and mast cells in the airways were identified by immunohistochemistry using a monoclonal antibody against tryptase and anti-IgE. The number of basophils of asthmatics was 52.2 +/- 12.5/mm(2). In contrast, no basophils were found in the airways of control subjects. There was a significant increase of number of mast cells in the asthma group compared to the control group (168.6 +/- 32.6 vs. 22.3 +/- 6.1, p<0.01). There was an inverse correlation between airway basophil and mast cell numbers and PC20ACh (r=-0.82, r=0.72, p<0.05). These findings suggest a possible role for basophils and mast cells in the pathophysiology of asthma.

Acetylcholine↗
PubMed1982

Blood eosinophil and basophil responses in guinea pigs parasitized by Amblyomma americanum ticks.

Guinea pigs sensitized to tick feeding by a previous infestation express immune resistance when challenged. This state is associated with large accumulations of eosinophils, and especially of basophils, at cutaneous sites of tick feeding. The present study shows that primary and secondary tick feeding stimulate blood eosinophilia and basophilia that reflect the infiltration of these cells in the skin. Primary feeding of Amblyomma americanum larvae resulted in a mean tick yield of 81%, mean tick weight of 0.91 mg and a feeding period of 3-5 days. Blood eosinophils and basophils began to rise on day 2 and reached peak 3-fold increases on day 4, the time of maximum tick drop-off. Secondary feedings 26 days later resulted in a mean tick yield of 45% (52% tick rejection), mean tick weight of 0.71 mg (22% weight decrease) and a mean feeding period of 4-6 days with maximum detachment on day 5. Prior to secondary tick feeding, both eosinophil and basophil levels were greater than in tick-free animals. Eosinophil levels peaked at day 4 to a level three times greater than in primary tick hosts. Basophil levels in secondary hosts exhibited minor elevations until day 6 when they were increased significantly, reaching a peak level of 33% higher than that observed in primary feedings. This study demonstrates that blood eosinophils and basophils respond quickly and significantly to primary tick feeding and undergo secondary responses of greater magnitude in response to subsequent tick challenge. However, challenge feeding resulted in a large blood eosinophilia with a modest blood basophilia. This may reflect the balance between bone marrow production and cutaneous accumulation of these cells at sites of tick rejection. Recruitment of eosinophils and basophils from the blood to the tissue site of tick feeding may contribute to the tick resistance mechanism.

Animals↗
PubMed2002

Differentiation of human basophils: an overview of recent advances and pending questions.

Basophils are rare, circulating leukocytes derived from hematopoietic CD34+ progenitors. The identification of cytokines promoting their development in vitro has led to substantial advances in understanding their differentiation process. An important role could be assigned to interleukin-3 (IL-3), which supports the maturation of hematopoietic progenitors into basophils in vitro and in vivo. In contrast to other myeloid lineages, a specific basophil growth factor has not yet been discovered. Furthermore, it is still unclear whether basophils possess a lineage-restricted progenitor or whether they share a common ancestor with mast cells (MC), eosinophils, or even megakaryocytes. Partial answers to these questions could be provided using in vitro culture systems or taking advantage of hematological disorders, such as chronic and acute myeloid leukemia (CML and AML), some myelodysplastic syndromes, and the very rare acute basophilic leukemia in which basophilic differentiation occurs.

Basophils↗
PubMed2002

GM-CSF and IFN-gamma-induced expression of human leucocyte antigen class II molecules on basophils of umbilical cord blood.

AIM: To determine whether basophils expressed human leucocyte antigen (HLA) class II molecules. METHODS: Basophils in umbilical cord blood were separated and purified with methods of density gradient centrifugation and immunomagnetic microbeads. The isolated basophils were cultured in RPMI-1640 plus 10 % fetal calf serum at 37 in a humidified atmosphere with 5 % CO2 and stimulated with granulocyte-macrophage colony-stimulating factor (GM-CSF) or interferon (IFN)-gamma for 20-60 h. The expression of HLA class II molecules on basophils was measured with fluorescence activated cell sorter (FACS). RESULTS: The purity of isolated basophils was > or = 83.5 %. After treated with GM-CSF 10 microg/L or IFN-gamma 100 kU/L, the expression of HLA class II molecules became detectable on membranous surface and at a higher level at 20 h, the percentage of expression was 10.2 %+/-2.1 % and 11.3 %+/-1.0 %, respectively. CONCLUSION: Basophils possessed the potency of HLA class II molecular expression.

Basophils↗
PubMed1992

Maitotoxin, a novel activator of mediator release from human basophils, induces large increases in cytosolic calcium resulting in histamine, but not leukotriene C4, release.

Maitotoxin (MTX) is a potent marine toxin which stimulates several Ca(++)-dependent processes presumably through an increase in Ca++ permeability. We have examined the effect of MTX on the release of chemical mediators from human basophils and its mechanism of action. MTX (1-20 ng/ml) induced histamine release (37-100%) from both mixed leukocyte preparations and purified basophils. Histamine release activated by MTX was slow (t 1/2 approximately equal to 15 min), temperature and Ca++ dependent (optimal at 37 degrees C and 1-2.5 mM Ca++). Sr++ ion could substitute for Ca++ in the secretory process. Digital video microscopy analysis of purified (> 70%) basophils revealed that MTX (1-20 ng/ml) induced a slow and marked increase of cytosolic Ca++ levels that was temporally coincident with histamine release. MTX (1-20 ng/ml) stimulated the release of sulfidopeptide leukotriene C4 from mixed leukocyte preparations (approximately equal to 0.5% basophils). However, purified basophils (77 +/- 7%) showed no sulfidopeptide leukotriene C4 release even in the presence of large histamine secretion (84 +/- 14%). Two organic Ca(++)-channel entry blockers, verapamil and diltiazem (1-30 microM) inhibited the release of histamine induced by MTX, whereas the dihydropyridine nifedipine (0.1-10 microM) caused only minimal inhibition. These results suggest that MTX represents a novel stimulus useful to study the role of Ca++ in human basophil mediator release.

Basophils↗
PubMed2003

Does skin prick test correlate with basophil-associated mite-specific IgE in atopic children?

Skin prick test (SPT), as the standard diagnostic tool for immediate hypersensitivity to aeroallergens, is an expression of IgE-dependent mediator release from dermal mast cells. Though probably involved in the late-phase response, peripheral blood basophils (PBB) don't seem to participate in the immediate hypersensitivity response in the skin. We aimed to assess a possible correlation between the SPT to mites and levels of basophil-associated mite-specific IgE. We sequentially enrolled 15 children with allergic rhinitis and documented class > II mite sensitization, mean age 13 years (range 9.5-18), 11 males, 4 females. Symptoms score was determined using a validated questioner. SPT area under the curve (AUC) for 10 common respiratory allergens was measured in all patients. Heparinized blood after basophil enrichment, was lysed with CHAPS. Determination of allergen-specific and total IgE in serum and cell lysate supernatant was performed using standard commercial kits. Basophil-associated, mite-specific IgE could be reliably determined only in 10 patients with a skin reaction greater than 70 mm2, OR 36 (95% CI 1.8-732, p = 0.02). We found a strong linear correlation (R2 = 0.74, p = 0.001) between mite-specific basophil-associated IgE density (IgE molecules per cell) and the SPT AUC. This finding suggests that skin mast cell precursors and basophil both bind specific IgE at a common site prior to the arrival of mast cells to the skin.

Adolescent↗
PubMed1992

Effect of IL-3 and stem cell factor on the appearance of human basophils and mast cells from CD34+ pluripotent progenitor cells.

Hemopoietic stem cell factor (SCF), which is the ligand for the proto-oncogene c-kit receptor (allelic with W locus) and the product of Sl locus of the mouse, has recently been cloned. The human homologue has also been cloned, and recombinant protein (human rSCF) expressed and purified to homogeneity. To determine the effect of human rSCF in the presence or absence of human rIL-3 on human bone marrow-derived mast cells and basophils, human CD34+ pluripotent progenitor cells, highly enriched (greater than 99%) from bone marrow mononuclear cells, were cultured over agarose surfaces (interphase cultures) in the presence of human rIL-3, human rIL-3 and increasing concentrations of human rSCF, or human rSCF alone. Over 3 to 4 wk, human rSCF acted synergistically with human rIL-3 at all concentrations, producing a three- to fivefold increase in total, mast cell, and basophil numbers over human rIL-3 alone when used at 100 ng/ml. The percentage of cell types in the human rIL-3 and human rIL-3 plus human rSCF cultures, however, remained the same, with basophils constituting 18 to 35% of the final cultured cells, and mast cells 3% or less of the final cell number. In the presence of human rSCF alone, the combined total percentage of mast cells and basophils was 0 to 1.0%, the majority of cells being macrophages. Mast cells cultured in human rIL-3 plus human rSCF, but not human rIL-3 alone, were berberine sulfate positive, suggesting the presence of heparin proteoglycans within granules. Electron microscopic examination of cultures supplemented with human rIL-3 and rSCF, but not human rIL-3 alone, revealed that after 3 wk in culture, mast cell granules contained tryptase and exhibited scroll, reticular, and homogeneous patterns as seen previously in CD34+/3T3 fibroblast cocultures. Thus, CD34+ cells cultured in the presence of both human rIL-3 and rSCF give rise to cultures containing increased numbers of basophils and mast cells, with the mast cells by ultrastructural studies showing evidence of maturation although the percentages of basophils and mast cells arising in these cultures remained unchanged.

Basophils↗
PubMed1992

Histamine-containing cells obtained from the nose hours after antigen challenge have functional and phenotypic characteristics of basophils.

The pattern of mediators and appearance of cells that stain with alcian blue during human experimental early and late phase allergic reactions suggest that basophils accumulate in nasal secretions within hours of local Ag stimulation. To further explore whether the histamine containing cells that enter the nose after Ag challenge are mast cells or basophils, we studied their functional and phenotypic characteristics. Approximately 24 h after intranasal Ag provocation of subjects with allergic rhinitis, nasal lavage was performed, and the cells were isolated for degranulation studies, analysis of surface Ag, and viability. The average histamine content per alcian blue staining cell was 0.78 +/- 0.2 pg (n = 7), similar to that reported for peripheral blood basophils. Nasal cells were challenged in vitro with anti-IgE, ragweed Amb a I, and FMLP and their responses were compared to those of peripheral blood basophils isolated simultaneously from the same donors. Nasal leukocytes released histamine maximally at 0.1 micrograms/ml of anti-IgE (35.8 +/- 7.8%, n = 7) and responded to FMLP (25.4 +/- 9.9%, n = 7). The response of the cells to ragweed Amb a I and anti-IgE was attenuated compared to peripheral blood basophils. Anti-IgE-induced histamine release was calcium and temperature dependent. Dual color immunofluorescence and flow cytometric analysis of the recovered nasal cells coexpressed CD18, a leukocyte marker not expressed by mast cells. The nasal cells consistently had high levels of spontaneous histamine release (19.5 +/- 2.0%, n = 22). The viability of all cells, assessed by erythrosin B dye exclusion, was 70 +/- 2% (n = 15). However, the viability of IgE-bearing cells was only 28.3 +/- 5.7% (n = 4). The characteristics of histamine release and the nature of the cellular surface markers provide functional proof that the histamine-containing cells accumulating after nasal Ag challenge are basophils and not mast cells.

Adult↗
PubMed1992

Activation of human basophils through the IL-8 receptor.

IL-8 and its structural analogs derived from blood platelets have been proposed as stimuli of IgE-independent basophil activation. In order to clarify the mechanism of action of these peptides, we examined the effects of pure IL-8, connective tissue-activating peptide III (CTAP-III), neutrophil-activating peptide 2 (NAP-2), and platelet factor 4 (PF-4) on blood basophils with and without pretreatment by IL-3, which modulates mediator release. After pretreatment with IL-3, significant histamine release was observed with 10(-8) M and 10(-7) M IL-8 and 10(-7) M NAP-2, but not with the other peptides. At higher concentrations (10(-6) M), however, all IL-8 analogs, as well as the unrelated cationic peptides poly-D-lysine, histone VS, and lysozyme, induced histamine release to variable degrees. Binding and competition studies with [125I]IL-8 revealed specific IL-8R on basophils from a patient with chronic myelogenous leukemia and normal individuals. From 3500 to 9600 receptors with a mean Kd value of 0.15 nM were found on average per chronic myelogenous leukemia and normal basophil, respectively. NAP-2 weakly competed for IL-8 binding. IL-8 and, to a lesser extent, NAP-2 led to a transient rise of cytosolic free calcium concentration ([Ca2+]i), which was independent of a preexposure to IL-3. IL-8 prevented the [Ca2+]i rise induced by NAP-2, but did not influence [Ca2+]i responses to other agonists, e.g. C5a, C3a, or platelet-activating factor. IL-8 induced [Ca2+]i changes and histamine release in IL-3-primed basophils were pertussis toxin sensitive. CTAP-III or PF-4 did not compete for IL-8 binding, did not induce [Ca2+]i changes, and did not influence the [Ca2+]i response to IL-8 and NAP-2. This study shows that IL-8 and NAP-2 activate human basophils by a receptor-mediated mechanism similar to that operating in neutrophils. At high concentrations histamine release can also be induced by cationic peptides by a mechanism that does not involve the IL-8R, and probably depends on cationic interactions.

Amino Acid Sequence↗
PubMed1992

Effect of nerve growth factor on the release of inflammatory mediators by mature human basophils.

Nerve growth factor (NGF) is a neurotrophic cytokine known to regulate the survival and function of peripheral and central neuronal cells. Recently, the spectrum of action could be extended to non-neuronal cell types such as rat mast cells and human B lymphocytes. The present study shows that NGF affects the function of mature human basophils isolated from the peripheral blood of healthy donors. Both murine NGF 7S and recombinant human NGF beta enhance histamine release and strongly modulate the formation of lipid mediators by basophils in response to various stimuli. This priming effect of NGF on basophils occurs rapidly within 10 to 15 minutes of preincubation, is dose-dependent, and requires similarly low concentrations (1 to 40 pmol/L) of human NGF beta as the induction of neurite outgrowth in ganglion cells. Cell fractionation studies indicate that NGF acts directly on human basophils without an involvement of other cell types, suggesting the presence of high-affinity NGF receptors on basophils. NGF by itself (up to 4 nmol/L of human NGF beta) does not induce the release of inflammatory mediators directly. The effect of human NGF on basophil mediator release is similar to that of the hematopoietic growth factors interleukin-3, interleukin-5, and granulocyte-macrophage colony-stimulating factor. The present study further demonstrates that NGF acts as a pleiotropic cytokine at the interface between the nervous and the immune system, and that NGF may be involved in inflammatory processes and hypersensitivity reactions.

Basophils↗
PubMedDate not supplied

Effect of allergen-specific immunotherapy on recombinant human interleukin 3-mediated amplification of allergen-induced basophil histamine release.

Decreased allergen-induced histamine release from peripheral blood basophils in allergic rhinitis patients treated with specific immunotherapy (SIT) correlates with clinical outcomes of SIT. The aim of this study was to investigate if decreased histamine release is a permanent effect of SIT. Fifty-one patients (mean age, 35.3 years) with allergic rhinitis, diagnosed based on clinical history and positive skin-prick test results to common aeroallergens, were studied. Twenty-three patients had never received SIT (group A), and 28 patients had been treated with inhalant allergen extracts (group B). Eleven patients from group A participated in a prospective part of this study. Basophil histamine release in these patients was evaluated before (TO) and after-1 year (TI) of SIT. Histamine release from peripheral blood with and without interleukin (IL)-3 pretreatment was performed using the glass-fiber-based histamine release test. Brief pretreatment of whole blood basophils with one of the four concentrations (0.01, 0.1, 1, or 10 ng/mL) of recombinant human IL(rhIL)-3, rhIL-5, or rh-granulocyte-macrophage colony-stimulating factor resulted in a significant amplification of allergen-induced basophil histamine release. The amplification using cytokines at the optimal concentrations was the greatest with rhIL-3 and the lowest with rhIL-5; therefore, for further studies rhIL-3 was used. Prospective analysis showed no significant difference in allergen-induced basophil histamine release on rhIL-3 pretreatment after 1 year of SIT (192.7 +/- 75.3 ng and 176.1 +/- 76.4 ng for T0 and T1, respectively; p = 0.18). Short-term SIT does not decrease rhIL-3-mediated amplification of allergen-induced histamine release from peripheral blood basophils.

Adolescent↗
PubMed2006

In vitro basophil activation using CD63 expression in patients with bee and wasp venom allergy.

The diagnosis of insect venom allergy and the indication for specific immunotherapy is based on history, skin tests and demonstration of hymenoptera venom-specific IgE-antibodies. Cellular tests can add useful information but the role of basophil activation tests for the different venoms has to be elucidated further. We evaluated positive reactions in a basophil activation test using CD63 expression as marker independently for bee or wasp venom in patients with hymenoptera allergy. Fifty-seven patients with a history of insect venom anaphylaxis were examined (12 x bee venom, 39 x wasp venom, 6 x bee plus wasp venom). Skin tests and determination of specific IgE-antibodies were performed. Basophil activation test (BAT) using CD63 expression was performed after stimulation with different concentrations of bee and wasp venom. The BAT is based on double staining with anti-IgE antibodies and anti-CD63 and subsequent determination of the percentage of activated basophils by flow cytometry. In patients with bee venom allergy, BAT was positive in 100% to bee venom and 75% to wasp venom. In patients with bee and wasp venom allergy, positive reactions for both venoms were found in 100%. In patients with wasp venom allergy, 97% reacted positive to wasp venom and only 56% to bee venom. These results show the reliability of the basophil activation test as a cellular test in the in vitro diagnosis in patients with bee and wasp venom allergy. They also show that positive reactions in the basophil activation test reflect both sensitization status and cross-reactivity between venom species.

Adolescent↗