Expression of sCD23 in atopic and nonatopic blood donors: correlation with age, total serum IgE, and allergic symptoms

Although structure, biologic activities, and expression of the low-affinity IgE receptor (Fc_eRII, CD23) have been investigated, the diagnostic value for allergies of this molecule and its soluble circulating fragment (sCD23) remains unclear. Therefore, serum sCD23 levels were measured in 203 blood donors. They were divided into atopic and nonatopic subjects by allergy history, physical findings of allergic symptoms, and corresponding specific circulating IgE antibodies. The group consisting of nonatopic subjects was divided into four age categories in order to exclude age-dependent variations in the expression of the low-affinity IgE receptor. In our study population, sCD23 serum levels were not influenced by age. Furthermore, no significant differences, especially no decrease in serum sCD23 levels, between the four nonatopic age groups were detected. There was no significant increase of sCD23 serum levels in atopic subjects in comparison with nonatopic blood donors. In addition, no correlation between total IgE levels and sCD23 serum levels could be detected, in either the group of atopic donors or the group of nonatopics. Our data suggest that the circulating low-affinity IgE receptor does not appear to be an additional general marker for the diagnosis of allergies, as previously suggested.     

Soluble CD23 in allergic diseases.

CD23, a differentiation marker of B cells is identified with the low-affinity receptor for IgE--FcepsilonRII. The CD23 molecule is continuously cleaved by autoproteolysis into soluble fragments called sCD23, considered as a multifunctional cytokine. sCD23 is supposed to play an important role in IgE synthesis. IgE is a hallmark of atopy and its overproduction is a characteristic feature of allergic diseases. The aim of this study was to determine sCD23 (25 kDA) serum levels in patients with inhalant allergy and hymenoptera venom-induced allergy with relevance to IgE system. The trial consisted of 18 patients with pollinosis, 25 with house dust mite allergy and 12 with hymenoptera venom-induced allergy. Eighteen healthy volunteers without signs of atopy served as a control group. Serum levels of sCD23 (25 kDa), total IgE and allergen specific IgE were measured as well. The results were presented as median value, 25-75% range and a total value range. Nonparametric tests (the U Mann-Whitney test, Kruskal and Wallis test and Spearman's correlation rang test) were used. In patients with allergic disorders serum levels of sCD23 were significantly higher than in the control group (p<0.05). No correlation between IgE levels and sCD23 was detected in all the investigated groups. sCD23 does not appear to be a hallmark of allergic diseases, however serum level of that molecule is significantly elevated in patients suffering from allergic disorders. No correlation between sCD23 and IgE has been observed. sCD23 serum level has no relevance to the types of allergic diseases.     

Serum CD23 is not altered in gastroallergic anisakiasis, but correlates with the production of specific IgE and the amount of polyclonal stimulation

BACKGROUND: Previous studies have shown elevated serum levels of the cytokines IL-4 and sCD23 in atopic patients and parasitic disease. Gastroallergic anisakiasis is an acute parasitic disease, accompanied by IgE-mediated clinical symptoms and an important increase of specific and total IgE. METHODS: Sixteen patients with acute urticaria/angioedema due to parasitism by Anisakis simplex after intake of raw or undercooked fish were selected, and serum samples were taken in the emergency room within 24 h (day 0; n=16), after 1 month (n=16), and after 6 months (n=10). Serum samples were studied for specific IgE against A. simplex, total IgE, sCD23, and IL-4. RESULTS: Mean values for sCD23 did not change in the observation period. Only 4/16 serum samples showed measurable IL-4 levels. Specific IgE and total IgE levels were found to be elevated after 1 month; after 6 months, they fell to nearly basal values. There was a positive correlation between sCD23 and specific IgE at day 0 and follow-up (r=0.55-0.69, P<0.026); a positive correlation between sCD23 and total IgE (r=0.54-0.62, P<0.056). Basal sCD23 could moderately predict the percentual increment of total IgE in the first month (r=0.56, P<0.038). CONCLUSION: Thus, it seems that interindividual variability of sCD23 is an important factor, with higher values predisposing to more production of unrelated IgE, independently of the parasite's action.     

Soluble CD23 potentiates interleukin-1-induced secretion of interleukin-6 and interleukin-1 receptor antagonist by human monocytes

The low-affinity receptor for IgE (CD23) is cleaved into biologically active soluble fragments (sCD23), some of which have been reported to exhibit pleiotropic activities. However, it is not known whether the sCD23 fragments contribute to the induction and/or regulation of pro-inflammatory cytokine production. In this study, this possibility was tested using interleukin (IL)-1-stimulated human whole blood as an ex vivo model of cytokine cascade production. We show that human recombinant 25-kDa sCD23 significantly enhanced the production of IL-6 in whole blood stimulated by IL-1, but had only little or no effect in the absence of IL-1. The potentiating effect of sCD23 was concentration dependent within the range of plasma levels occurring during various inflammatory processes in man. These results prompted us to study whether sCD23 and IL-1 together also enhance the production of regulating factors exhibiting anti-cytokine activities. Our data indicate that sCD23 augments the release of IL-1 receptor antagonist induced by IL-1. Finally, examining the effect of sCD23 on human peripheral monocytes stimulated by IL-1, we confirmed the capacity of sCD23 to potentiate cytokine production. We suggest that sCD23 can modulate monocyte functions, thereby contributing to the amplification and regulation of immune and inflammatory processes.     

Markedly high eosinophilia and an elevated serum IL-5 level in an infant with cow milk allergy.

BACKGROUND: Interleukin-5 (IL-5) promotes the production and function of eosinophils, and an increase in the serum soluble CD23 (sCD23) level is suggestive of enhanced type-2 helper T-cell activity. The secretion of a large amount of the proinflammatory cytokine, tumor necrosis factor alpha (TNF-a), has been reported to alter the intestinal barrier capacity. OBJECTIVE: To determine whether or not distinct profiles of cytokine production were involved in the marked peripheral eosinophilia of as high as 20,000/mm3 and the gastrointestinal symptoms seen in an infant with cow milk allergy. METHODS: The levels of IL-5, sCD23, and TNF-alpha in serum and the culture supernatants of mononuclear cells were compared with those in infants with anaphylaxis to cow milk and nonallergic infants. RESULTS: Interleukin-5 was detected in the serum (19 pg/mL) but became undetectable after 2 weeks on a milk-free diet together with clinical remission. A kinetic decrease in the serum sCD23 level was also observed during the administration of a milk-free diet with improvement of the eosinophilia in 2 months. The TNF-alpha produced in vitro after stimulation with cow milk protein was not different from in controls. CONCLUSION: It seems likely that the allergic inflammation due to cow milk can induce marked eosinophilia with an associated increase in IL-5 production.     

Circulating elevated levels of soluble CD23, interleukin-4, and CD20+CD23+ lymphocytes in atopic subjects with elevated serum IgE concentrations.

Circulating IgE protein levels, leukocyte counts, lymphocyte subsets, IL-4, and soluble CD23 levels were quantitated in 43 atopic and 19 nonatopic subjects. Mean values of IgE protein levels, total eosinophil counts, CD20+CD23+ cells (B cells with low-affinity IgE receptor), IL-4 and sCD23 levels were elevated in atopic patients compared with nonatopic controls. The results suggest that sCD23, IL-4, and CD20+CD23+ lymphocytes may play a role in the increased production of IgE in atopic subjects in a manner similar to that observed by other investigators in prior in vitro studies.     

Chemokines, sTNF-Rs and sCD30 serum levels in healthy aged people and centenarians

Several lines of evidence point to a profound remodelling of the cytokine network in healthy elderly subjects, with decreased type-1 cytokine production (IL 2) and a shift to type 0 and 2. We have also observed an increase of proinflammatory cytokines (IL-1, IL-6, TNF-alpha) in vitro, and an increase of circulating stem cell factor in vivo. In this setting, we studied changes of chemokines (MCP-1 and RANTES) with aging, as well as other molecules, namely, sTNF-RI and sTNF-RII, and the soluble form of the CD30 molecule (sCD30), involved in the pro- and antiinflammatory cytokine balance. The subjects enrolled in the study belonged to three different selected healthy groups of young, aged and centenarians. The presence of rheumatoid factor (RF) and antinuclear antibodies (ANA) was simultaneously assessed. The results show that MCP-1 serum levels were higher in the healthy aged and lowest in the young, while RANTES increased exclusively in centenarians. Only centenarians had autoantibodies (ANA and RF). sTNF-RI and sTNF-RII were significantly elevated in healthy old subjects compared to the young, and even higher in selected centenarians compared to the other age groups. sCD30 serum levels were significantly raised in centenarians compared to the young, despite absence of circulating CD30+ cells in the peripheral blood of the whole study population. No relationship among serum values of these different members of the TNF-R family was found, despite a strong correlation for sTNF-RI and sTNF-RII in all groups. We hypothesize that the increased chemokine levels in aged people, and raised sCD30 levels in centenarians, may reflect a general shift towards type 0/2 cytokines in normal aging, which may be responsible, at least in part, for the appearance of circulating autoantibodies without definite clinical consequences at advanced age.     

Developmental changes in interleukin-12-producing ability by monocytes and their relevance to allergic diseases

BACKGROUND: The T helper type-2 (Th2)-dominated situation can be observed in allergic diseases such as asthma or atopic dermatitis. A reduced ability to produce IL-12, which is a key cytokine for the induction of Th1 responses, has been proposed to lead to aberrant Th2 development in these disease conditions. OBJECTIVE: This study was intended to examine how IL-12-producing ability might associate with allergic diseases as a function of age. METHODS: IL-12 production by monocytes at various ages was assessed in patients with bronchial asthma and/or atopic dermatitis (n = 100) in comparison with non-allergic control subjects (n = 144). Whole blood cells were stimulated with lipopolysaccharide (LPS) after priming with IFN-gamma, then intracellular cytokine expression of IL-12 and IL-8 as a control cytokine of CD14-positive cells was assessed by flow cytometric analysis. RESULTS: In the control subjects, the ability of monocytes to produce IL-12 was negligible at birth and gradually increased with advancing age, whereas IL-8 production was intense throughout the human life. At more than 7 years of age, IL-12 production of patients with allergic diseases was significantly lower compared with that of control subjects. The unexpected finding was that infants and children below 6 years of age with allergic diseases tended to produce more IL-12 compared with age-matched controls. In this young group, it was noted that enhanced IL-12 production by monocytes was especially observed in allergic patients with specific IgE antibodies against some food allergens. Significant inverse relationships between serum IgE levels and IL-12-producing ability were found in the teenage and adult groups, but not in the younger children. CONCLUSION: IL-12 appeared to play different roles in the pathogenesis of allergic diseases between younger and older ages.     

Inhibition of CD23 processing correlates with inhibition of IL-4-stimulated IgE production in human PBL and hu-PBL-reconstituted SCID mice

BACKGROUND: CD23, the low affinity serum immunoglobulin E (IgE) receptor, is upregulated on B cells following interleukin (IL)-4 stimulation and is concomitantly cleaved to generate soluble CD23 (sCD23) fragments with cytokine-like activity. OBJECTIVE: Compounds that selectively inhibit the proteolytic release of CD23 to generate sCD23 were assessed for their ability to inhibit IgE production in order to evaluate the contribution of sCD23 in the production of human IgE as well as the ability of such compounds to block IgE production. METHODS: IgE production was measured in IL-4-stimulated human peripheral blood lymphocytes (PBL) and PBL-reconstituted SCID mice in the presence of a broad-spectrum matrix metalloprotease (MMP) inhibitor, a compound selective for inhibition of CD23 processing over MMPs and an anti-CD23 mAb, MHM6. RESULTS: The two compounds were equipotent in inhibiting IgE production without inhibition of IgG production by IL-4/anti-CD40-stimulated PBL. Soluble CD23 release was also shown to precede IgE accumulation in the cell-free medium. Addition of compound at later times other than day 0 in the 14 day assay resulted in progressively less inhibition of both IgE and sCD23, and exactly paralleled the effect of an anti-CD23 mAb, MHM6 on IgE levels. Both compounds also inhibited the release of CD23 from human RPMI 8866 cells adoptively transferred i. p. to mice. Doses required for inhibition of CD23 correlated well with the doses required for inhibition of IgE production in IL-4-challenged hu-PBL-SCID mice. IgE was selectively inhibited over total IgG in the SCID mice as well. CONCLUSIONS: Inhibition of CD23 processing alone is sufficient to inhibit IL-4-stimulated IgE production both in vitro and in vivo.     

Soluble CD23 (sCD23) serum levels and lymphocyte subpopulations in peripheral blood in rhinitis and extrinsic and intrinsic asthma

To determine serum levels of IgE and sCD23 and lymphocyte subpopulations, we studied 37 control subjects and 84 patients (27 with allergic rhinitis, 27 with extrinsic asthma, and 30 with intrinsic asthma). A rise in surface CD23 on B and monocyte cells and sCD23 serum levels was exhibited by patients with rhinitis and extrinsic asthma. Unexpectedly, in intrinsic asthmatic patients, high CD23 expression on monocytes and high sCD23 levels were seen that did not result in IgE production. It appears that CD23, in its soluble form, could be a good disease marker, especially in asthma. Atopic patients yielded a significantly lower proportion of CD4⁺ T cells than intrinsic asthmatic patients and normal persons. Otherwise, CD4⁺ CD29⁺ CD45RA - and CD4⁺ CD29 – CD45RA ⁺ T-cell subsets were significantly decreased in all patient groups.     

Chemokines,sTNF-Rs and sCD30 serum levels in healthy aged people and centenarians

Several lines of evidence point to a profound remodelling of the cytokine network in healthy elderly subjects, with decreased type-1 cytokine production (IL 2) and a shift to type 0 and 2. We have also observed an increase of proinflammatory cytokines (IL-1, IL-6, TNF-α) in vitro, and an increase of circulating stem cell factor in vivo. In this setting, we studied changes of chemokines (MCP-1 and RANTES) with aging, as well as other molecules, namely, sTNF-RI and sTNF-RII, and the soluble form of the CD30 molecule (sCD30), involved in the pro- and antiinflammatory cytokine balance. The subjects enrolled in the study belonged to three different selected healthy groups of young, aged and centenarians. The presence of rheumatoid factor (RF) and antinuclear antibodies (ANA) was simultaneously assessed. The results show that MCP-1 serum levels were higher in the healthy aged and lowest in the young, while RANTES increased exclusively in centenarians. Only centenarians had autoantibodies (ANA and RF). sTNF-RI and sTNF-RII were significantly elevated in healthy old subjects compared to the young, and even higher in selected centenarians compared to the other age groups. sCD30 serum levels were significantly raised in centenarians compared to the young, despite absence of circulating CD30+ cells in the peripheral blood of the whole study population. No relationship among serum values of these different members of the TNF-R family was found, despite a strong correlation for sTNF-RI and sTNF-RII in all groups. We hypothesize that the increased chemokine levels in aged people, and raised sCD30 levels in centenarians, may reflect a general shift towards type 0/2 cytokines in normal aging, which may be responsible, at least in part, for the appearance of circulating autoantibodies without definite clinical consequences at advanced age.     

Distinct modulation by interferon-gamma (IFN-γ) of CD23 expression on B and T lymphocytes of atopic subjects

The low-affinity IgE receptor (FcεRII/CD23) plays a role in IgE production. Cytokines participating in IgE synthesis also modulate CD23 expression on lymphocytes, but whether this modulation is different in atopic subjects remains unclear. We studied CD23 expression on B and T lymphocytes in 10 asthmatic patients with Dermatophagoides pteronyssinus hypersensitivity and 10 healthy non-atopic subjects. Studies were performed by flow cytometry, in phytohaemagglutinin (PHA) or IL-4-stimulated mononuclear cell cultures, alone or in the presence of IFN-γ. Soluble CD23 (sCD23) released in the culture supernatants was measured by enzyme-linked immunoassay. Both PHA and IL-4 induced the expression of CD23 on lymphocytes of atopic and non-atopic subjects. Whereas PHA increased both the percentage and mean fluorescence intensity of CD23⁺ B and T cells, IL-4 alone did not increase the percentage of CD23⁺ T cells. The effects of IFN-γ were different in both groups, since it was able to reduce the percentage of PHA-stimulated CD23⁺ T cells only in non-atopic individuals. In non-atopic subjects more than atopic, levels of sCD23 were increased in the supernatants of PHA and IL-4 cultures. These results show that the modulation of CD23 expression is different on B and T cells, and that IFN-γ acts differently in atopic and non-atopic individuals.     

IgE secretion is attenuated by an inhibitor of proteolytic processing of CD23 (FcεRII)

CD23, the low-affinity IgE receptor, is up-regulated on interleukin (IL)-4-stimulated B cells and monocytes, with a concomitant increase in the release of soluble fragments of CD23 (sCD23) into the medium by proteolytic processing of the surface-bound intact CD23. The effect of inhibition of the processing of CD23 on IgE production in human and mouse cells and in a mouse model in vivo was evaluated. CD23 processing to sCD23 from RPMI 8866 (a human Epstein-Barr virus-transformed B cell line) cell membranes was inhibited by a broad-spectrum matrix-metalloprotease inhibitor, batimastat, with an IC₅₀ of 0.15 μM. Batimastat also inhibited CD23 processing in whole RPMI 8866 cells as well as in IL-4-stimulated purified human monocytes with similar IC₅₀. Batimastat inhibited IgE production from IL-4/anti-CD40-stimulated human tonsil B cells as well as mouse splenic B cells in a manner consistent with inhibition of CD23 processing. Release of soluble fragments of CD23 in the cell supernatants of tonsil B cells was inhibited over the concentration range of 1–10 μM batimastat and intact cell surface CD23 was increased on mouse splenic B cells in the presence of these concentrations of batimastat. IgE production of IL-4-stimulated human peripheral blood mononuclear cells was also blocked by 1–10 μM batimastat, again with comparable inhibition of sCD23 release over the same concentration range. Finally, in a mouse model of IgE production, batimastat inhibited IgE production in response to ovalbumin challenge as determined by serum IgE levels. Taken together, the data support a role of CD23 in IgE production and point to CD23 processing to sCD23 as a therapeutically relevant control point in the regulation of IgE synthesis.     

Serum levels of interleukin-4, soluble CD23 and IFNγ in relation to the development of allergic disease during the first 18 months of life

Serum levels of Interleukin (IL)-4, Interferon (IFN)-γ and soluble CD23 (sCD23) were analysed in a prospective study of 64 infants who were monitored from birth to 18 months of age. The findings were related to family history of atopy and the development of allergic disease in the infants. Low levels of IL-4 were detected in 10 of 63 cord blood samples (median 0.14 and range 0.32 μg/1). The levels then increased, both in healthy and atopic infants, reaching a peak at either 6 or 9 months and then decreased up to 18 months of age. The children who developed atopic disease during the first 18 months of life had significantly higher IL-4 median levels than those who did not, i.e. 0.24 (range 0.40) vs <0.10 μg/1 at 3 months, (P< 0.001), 0.40 (range 0.95) vs 0.13 (0.19) μg/1 at 6 months (P < 0.01), 0.46 (range 0.78) vs 0.10 (0.24) μg/1 at 9 months (P< 0.001) and 0.30 (range 1.38) vs 0.10 (0.36) μg/1 at 18 months (P< 0.001). The IFNγ levels were below the detection level, i.e. < 100 ng/1 in all but 49 of the 196 serum samples that were analysed. There was no significant relationship with clinical outcome, nor with S-IgE levels. Soluble sCD23 levels increased in the infants with age. There was no association with either atopic disease, family history of allergic disease or IgE antibody levels. In conclusion, IL-4 levels in serum, but not sCD23 and IFN7 are associated with allergic disease in infancy. Elevated levels were recorded before the onset of clinical symptoms. The findings support that atopic disease is associated with a primary abnormality of T-cell function.     

Soluble CD21 (sCD21) forms biologically active complexes with CD23: sCD21 is present in normal plasma as a complex with trimeric CD23 and inhibits soluble CD23-induced IgE synthesis by B cells

A soluble form of CD21 (sCD21) of 135 kDa is spontaneously released by human B and T lymphocytes upon shedding of the extracellular domain of the molecule. By Western blotting, we have now identified two forms of sCD21 of Mr 135 and 90 kDa in normal human serum. We further demonstrate that sCD21 circulates in a complexed form with cleavage fragments of C3 and CD23, two previously identified ligands of the membrane CD21 receptor. The CD23 molecule was in the form of a trimer in the soluble complex purified from plasma by affinity chromatography on anti-CD21 Sepharose. The serum sCD21 complex was also found to contain IgE. The presence of IgE and of CD21 in a soluble complex that contains trimeric CD23 as the only form of soluble CD23 (sCD23) is in agreement with a model in which two of the three lectin heads of CD23 bind to the Cepsilon3 domain of IgE, thus leaving one of the heads available for interaction with CD21. We further demonstrate that sCD21 inhibits sCD23-induced IgE synthesis by IL-4-stimulated B cells. The results indicate that sCD21 in plasma retains the ligand-binding properties of the membrane CD21 receptor and exhibits immunoregulatory properties that may be relevant to allergic and inflammatory disorders.      

Serum IgE levels, atopy, and asthma in young adults: results from a longitudinal cohort study

To explore the natural history of asthma and its relation to allergic responses, we examined the relation between total serum IgE in early adulthood and a history of respiratory symptoms, airway hyperresponsiveness (AHR), and atopy during childhood. We studied 180 subjects aged 18–20 years who had been studied since the age of 8–10 years. We measured wheeze in the previous year by questionnaire, AHR by histamine inhalation test, atopy by skin prick tests, and serum IgE levels by immunoassay. Subjects with AHR in early adulthood had higher IgE levels (mean 257.0 IU/ml) than subjects with past AHR (mean 93.3 IU/ml) or with lifelong normal responsiveness (mean 67.6 lU/ml) ( P< 0.001). Subjects who had symptoms had higher IgE levels (mean 125.9 IU/ml) than those who were lifelong asymptomatic (mean 63.1 IU/ml) ( P< 0.001). Recent wheeze, AHR, and allergic sensitization all had a positive relation to serum IgE, but IgE was not more predictive of AHR than skin prick tests. The finding that young adults who are sensitized to common allergens are highly likely to have AHR even in the absence of symptoms is further evidence of the fundamental role of IgE-mediated responses in the natural history of AHR throughout childhood and into adulthood.     

The association between serum levels of Th cytokines and rhinoconjunctivitis caused by methyltetrahydrophthalic anhydride

Background There are few epidemiologic studies on the association between serum levels of T helper (Th) cytokines and allergic symptoms caused by sensitizing agents.
Methods A population of 147 workers from two condenser plants using epoxy resin with methyltetrahydrophthalic anhydride (MTHPA) underwent a questionnaire survey and serologic investigations. Total and MTHPA-specific IgE levels were measured by the Pharmacia CAP System, and serum levels of interleukin (IL)-4, IL-13, and interferon-gamma (IFN-γ) by enzyme immunoassay.
Results A significant association was found between work-related eye and nasal symptoms and a range of atopic characteristics, including the frequency of positive specific IgE, specific and total IgE levels, and IL-4 levels. A positive correlation was observed between levels of IL-4 and IL-13 (r=0.42). Furthermore, multiple logistic analysis revealed significant contributions of specific IgE and I H3 to the work-related symptoms. A similar but nonsignificant association was also found for IL-4 (P=0.07). On the other hand, a multiple regression model with specific IgE levels as a dependent variable showed a significant association with total IgE, but not with IL-4, IL-13, and IFN-γ.
Conclusions These results suggest that work-related eye and nasal symptoms are closely related to specific IgE antibodies, and that allergic responses, mediated by IgE, to MTHPA may lead to a shift in the balance between Thl and Th2 cells.     

Oral delivery of Lactobacillus casei Shirota modifies allergen-induced immune responses in allergic rhinitis

Background Changes in the composition of the gut microbiota have been implicated in the pathogenesis of allergic disorders, suggesting beneficial interactions between the intestinal immune system and specific bacterial strains. Lactobacilli are naturally present within the complex gastrointestinal microbiota of humans and they are currently present in many probiotic supplements.
Objective We sought to investigate the role that Lactobacillus casei Shirota (LcS) may play in modulating seasonal allergic rhinitis (SAR).
Methods The study format was double-blinded, placebo-controlled with 10 SAR sufferers in each group. We have documented and compared changes in immune status arising through the daily ingestion of a milk drink with or without live LcS, over a period of 5 months. Pre-, peak- and post-grass pollen season blood samples were collected for determination of plasma total IgE and grass pollen-specific IgG and IgE levels by an enzyme immunoassay. At the same time, cytokine levels were determined by flow cytometric bead array technology following culture of peripheral blood mononuclear cells for 6 days in the presence or absence of specific grass pollen antigens.
Results Volunteers treated with LcS showed a significant reduction in levels of antigen-induced IL-5, IL-6 and IFN-γ production compared with volunteers supplemented with placebo. Meanwhile, levels of specific IgG increased and IgE decreased in the probiotic group.
Conclusion Changes in antigen-induced production of cytokines were observed in patients treated with probiotics. These data show that probiotic supplementation modulates immune responses in allergic rhinitis and may have the potential to alleviate the severity of symptoms.     

Postsplenectomy Type-1 Hypersensitivity Response: A Correlation Between IL-4 and IgE Serum Levels

Authors demonstrated the presence of allergic manifestations in splenectomized patients following traumatic rupture of this organ. In particular, allergic diathesis, as supported by serum IgE increase, was exclusively found in patients with preserved T helper (h)-2 lymphocyte function. Th-2 function was monitored by measuring serum levels of interleukin (IL)-4, a cytokine involved in IgE synthesis. On the opposite, in splenectomized individuals with a reduced Th-2 function as supported by lower IL-4 serum levels, no IgE increase and allergic manifestations were detectable. On these grounds, authors hypothesize that allergic manifestations may be correlated to splenectomy since its exeresis may favor the persistence of antigens in the blood. Consequentially, in patients with a preserved Th-2 function, antigenic overload may lead to IgE increase and allergy onset.     

Postsplenectomy type-1 hypersensitivity response: a correlation between IL-4 and IgE serum levels

Authors demonstrated the presence of allergic manifestations in splenectomized patients following traumatic rupture of this organ. In particular, allergic diathesis, as supported by serum IgE increase, was exclusively found in patients with preserved T helper (h)-2 lymphocyte function. Th-2 function was monitored by measuring serum levels of interleukin (IL)-4, a cytokine involved in IgE synthesis. On the opposite, in splenectomized individuals with a reduced Th-2 function as supported by lower IL-4 serum levels, no IgE increase and allergic manifestations were detectable. On these grounds, authors hypothesize that allergic manifestations may be correlated to splenectomy since its exeresis may favor the persistence of antigens in the blood. Consequentially, in patients with a preserved Th-2 function, antigenic overload may lead to IgE increase and allergy onset.