Serum IgE Levels In Patients Research Articles

Both Th1 and Th2 chemokines are elevated in sera of patients with autoimmune blistering diseases

Although chemokines are critical elements for the selective attraction and activation of various leukocyte subsets in the inflammatory process, there are few findings concerning T helper (Th) 1 or Th2 chemokines in autoimmune blistering disease (ABD). To determine whether serum levels of chemokines that are preferentially chemotactic for Th1 (monokine induced by IFN-gamma (MIG/CXCL9)) and Th2 (thymus and activation regulated chemokine (TARC/CCL17) and macrophage derived chemokine (MDC/CCL22)) cells were elevated and whether they correlated with the clinical features in patients with ABD. Serum chemokine levels were examined using ELISA in patients with pemphigus vulgaris (PV, n=19), pemphigus foliaceous (PF, n=14), or bullous pemphigoid (BP, n=27) and normal controls (n=20). Serum MIG levels were significantly higher in patients with PV, PF, or BP than those in the control subjects. Serum levels of TARC and MDC were also significantly elevated in patients with PV, PF, or BP relative to the normal controls. Among the ABD subgroups, the levels of each chemokine tended to be higher in BP patients than in PV patients. Furthermore, serum TARC levels correlated positively with serum IgE levels in patients with ABD. Levels of TARC, MDC, and MIG were significantly decreased after treatment when the skin lesions disappeared in these patients. Furthermore, serum MIG levels correlated positively with serum levels of TARC and MDC in the ABD patients. These results suggest that both a Th1 chemoattractant MIG and Th2 chemoattractants, TARC and MDC, cooperatively play a role in the development of ABD.

Serum IgE levels in neurofibromatosis 1

A descriptive case study was performed on 75 patients with NF1 (neurofibromatosis type 1) from the CNNF (Brazil) database. Serum IgE levels were determined using the IgE radioimmunosorbent test, with the reference values of 75-502 IU mL(-1). The patients were divided into groups, with 25 patients presenting plexiform neurofibromas, 25 presenting neurofibromas and 25 presenting no neurofibromas. The purposes of this study were to determine the serum IgE levels of patients with NF1 presenting plexiform neurofibromas, neurofibromas and no neurofibromas, as well as to determine possible correlations between serum IgE levels and the size of the plexiform neurofibromas and neurofibromas presented by these patients. Elevated serum IgE levels were observed in all the patient groups. We did not observe a correlation between IgE levels and age in these patients; however, we did observe correlations between IgE levels and neurofibroma and plexiform neurofibroma size. We suggest further studies to confirm these results and to investigate in greater depth the possible role of IgE in the development and growth of neurofibromas and plexiform neurofibromas in NF1.

970. p53 Expression and Serum IgE Levels in Patients with Neurofibromatosis type 1

970. p53 Expression and Serum IgE Levels in Patients with Neurofibromatosis type 1

Expression of membrane-bound CD23 in nasal mucosal B cells from patients with perennial allergic rhinitis

CD23 is the low-affinity receptor for IgE on B cells and is thought to play an important role in regulation of IgE production. To measure the expression of membrane-bound CD23 in nasal B cells and examine its correlation with CD4 subtypes or serum IgE levels in patients with perennial allergic rhinitis. We used flow cytometric analysis with double, direct immunofluorescence staining of the mucosal-infiltrating lymphocytes to examine the expression of CD23 in nasal mucosal B cells of patients with perennial allergic rhinitis. The expression of CD23 in nasal B cells of patients with nonatopic rhinosinusitis served as a control. The ratio of CD23+ B cells to total B cells in patients with perennial allergic rhinitis was significantly higher than in nonatopic controls, whereas that of B cells to total lymphocytes was unchanged. The ratio of CCR4+ CD4 cells to total CD4 cells in allergic patients was significantly higher than in nonatopic controls, whereas the ratio of CXCR3+ CD4 cells to total CD4 cells was unchanged. There was no significant correlation between the percentages of CD23+ B cells and CCR4+ CD4 cells. In addition, the percentage of CD23+ B cells did not correlate with the total IgE level or with the specific IgE level. Our results indicate that nasal mucosal CD23-bearing B cells, as well as T(H)2 cells, increase in patients with perennial allergic rhinitis. However, the expression of CD23 did not directly correlate with the number of T(H)2 cells in the nasal mucosa.

IgE-Dependent Activation of T cells by Allergen in Atopic Dermatitis: Pathophysiologic Relevance

The importance of interactions between allergen and IgE in allergen-mediated activation of T lymphocytes from patients with atopic dermatitis (AD) is unclear. A role for this interaction is implied by past evidence for IgE-facilitated presentation of allergen to T cells, but this phenomenon has only been demonstrated in specific in vitro systems biased to maximize the effect. It is therefore not known whether the process is relevant in patients. We now show that the responses to allergen of unmodified peripheral blood mononuclear cells (PBMC) from individual AD patients are significantly greater in the presence of fresh, unheated, IgE-containing autologous serum than the same serum heated under IgE-denaturing conditions or specifically depleted of IgE by immunoprecipitation. In six independent experiments, 59%-67% of the maximal in vitro PBMC response to allergen was found to be dependent upon the presence of IgE in autologous serum used at 5% final concentration. These data provide the first evidence that sufficient amounts of allergen-specific IgE and allergen-reactive T cells occur concomitantly in the blood of individual AD patients to allow IgE-enhanced T cell responses to allergen. We conclude that IgE-enhanced T cell responses are pathophysiologically relevant and a therapeutic target in AD.

Serum IgE-levels in Patients with Chronic Sarcoidosis vs. Patients with Acute Disease and Healthy Controls

PURPOSE: The thesis on allergy and atopy in sarcoidosis patients has been present as a challenge considering different immunology pathways of sarcoidosis for years. The aim of this study is to present the correlation of the low serum IgE levels in patients with chronic sarcoidosis and the serum IgE levels of the healthy control subjects, and to introduce into the discussion different possibilities of the immune response in sarcoidosis.

Increased total serum IgE levels in patients with asthma and promoter polymorphisms at CTLA4 and FCER1B

Background: Increasing evidence indicates that total serum IgE levels are largely determined by genetic factors, and we recently established that the –109C/T promoter polymorphism at FCER1B is a genetic factor that affects total serum IgE levels. The gene encoding cytotoxic T lymphocyte antigen 4 (CTLA4) is another candidate factor in high IgE responsiveness, because B7-CD28/CTLA4 interaction can promote the differentiation and development of the T H2 lymphocyte subset. Objective: We intended to determine whether CTLA4 is associated with increased levels of total serum IgE or with the development of asthma or atopy. Methods: We performed a case-control study involving 339 patients with asthma and 305 healthy control subjects, of whom 226 of the patients with asthma and 219 of the healthy control subjects had previously been genotyped for the –109C/T promoter polymorphism at FCER1B. In the current study, we genotyped 2 polymorphisms in the CTLA4 gene, one involving the promoter (–318C/T) and the other involving exon 1 (+49A/G), in addition to the FCER1B promoter polymorphism. Results: Patients with asthma who were homozygous for the –318C allele at the CTLA4 promoter region had higher levels of total serum IgE than patients with asthma carrying the –318T allele ( P = .00470). The analysis of –318C/T (at CTLA4) and –109C/T (at FCER1B) promoter polymorphisms showed a significant correlation between the combined genotypes and increased levels of total IgE in patients with asthma ( P = .000014). In contrast, no correlation between total serum IgE levels and –318C/T or +49A/G genotypes was detected in 305 healthy control subjects. There was no evidence indicating an association between a putative allele for asthma or atopy and alleles at any of the CTLA4 polymorphic loci. Conclusion: Our findings suggest that promoter polymorphisms of both CTLA4 and FCER1B are genetic factors that influence total serum IgE levels in patients with asthma. This supports the theory that variance in total serum IgE levels in patients with asthma is determined by mutations in multiple genes, each of which has a relatively small effect on the phenotype. (J Allergy Clin Immunol 2001;108:74-9.)

Interleukin-18 Is Elevated in the Sera from Patients with Atopic Dermatitis and from Atopic Dermatitis Model Mice, NC/Nga

Background: Several lines of in vitro and in vivo studies have demonstrated that interleukin-18 (IL-18) shows both antiallergic and allergy-promoting activities. But its expression in allergic diseases remains unknown. Methods: Serum IL-18 levels from atopic dermatitis (AD) model mice, NC/Nga and control mice and from patients with AD and healthy volunteers were measured by ELISA. The relationship between IL-18 levels and serum IgE levels or clinical severity was also examined. Results: Serum IL-18 levels from NC/Nga mice were significantly increased compared to those from control mice. The elevation of IL-18 in the sera was observed prior to the onset and during the development of dermatitis in NC/Nga mice. In addition, IL-18 levels in the sera from patients with AD were significantly (p < 0.05) elevated compared to those from healthy volunteers. However, serum IL-18 levels tended to correlate negatively with serum IgE levels in patients with AD and NC/Nga mice. Conclusion: IL-18 is overexpressed in AD.

Total Serum IgE Levels in Chronic Hepatitis C: Influence of Interferon Alpha Therapy

Background: Liver disease has been considered a prominent cause of IgE elevation. No data on serum IgE levels in chronic hepatitis C have been reported. Interferon-α is a standard therapy for chronic hepatitis C. Cytokine use is a promising type of immunomodulation in the treatment of IgE-mediated diseases. The effects of interferon-α therapy on serum IgE have not been fully evaluated. The aim of the study was to evaluate both serum IgE levels in patients with chronic hepatitis C and the course of these levels after interferon-α therapy. Patients and Methods: Serum IgE was determined in 100 adult patients with chronic hepatitis C (24 atopics according to positive skin prick tests and 76 nonatopics) and in 75 healthy controls (25 atopics and 50 nonatopics). Serum IgE measurements were repeated at 1 and 3 months of therapy with recombinant interferon-α (3 × 106 units s.c. 3 times weekly) in 34 of these patients. Results: Serum IgE levels were similar in chronic hepatitis C patients and in controls when adjusted for atopic status. Among patients with chronic hepatitis C, serum IgE levels were unrelated to liver necroinflammatory activity. A modest but statistically significant increase of IgE values was observed after interferon-α therapy, particularly in patients with no virological response. Conclusions: Chronic hepatitis C is not a significant cause of increased total serum IgE values. Serum IgE increase in some patients with liver disease may be related to the cause of liver injury and not to liver disease per se. Interferon-α therapy in patients with chronic hepatitis C is followed by no modification or even a moderate increase of serum IgE values.

Increased urinary leukotriene E4 excretion in patients with atopic dermatitis.

Synthesis of cysteinyl leukotrienes (LTs) is known to play a part in the pathogenesis of inflammatory diseases. To define the involvement of cysteinyl LTs in atopic dermatitis (AD). Synthesis of cysteinyl LTs was assessed in patients with AD and healthy volunteers by measuring urinary LTE4, a useful index of systemic cysteinyl LT synthesis, using liquid chromatography/tandem mass spectrometry. Mean +/- SD urinary LTE4 levels in patients with AD (125 +/- 69 pg mg(-1) creatinine, n = 20) were significantly higher (P < 0.01) than in healthy volunteers (60 +/- 19 pg mg(-1) creatinine, n = 17). A significant correlation between urinary LTE4 and total serum IgE levels in patients with AD was observed (r = 0.643, P < 0.05). Our findings demonstrate an enhanced synthesis of cysteinyl LTs in patients with AD and suggest that cysteinyl LTs are involved in the pathophysiology of AD.

Serum IgE Levels in Patients with Human Immunodeficiency Virus Infection

Increased serum IgE levels are associated with advanced HIV infection. The magnitude of the increase has varied greatly between studies which generally did not assess potential confounding factors. To determine whether the increased serum IgE levels reported with HIV infection is affected by demographic or behavioral factors, we studied injection drug users, women, and minority ethnic and racial groups with HIV infection, for whom little data now exist. A prospective cross-sectional study of ambulatory patients with or at risk for HIV infection was performed. We enrolled 83 injection drug users and 56 non-drug users seropositive for HIV and 43 seronegative at-risk individuals from an Infectious Diseases clinic and a longitudinal study of HIV infection in injection drug users in the Bronx, New York City. Fifteen HIV-seronegative non-atopic controls were also studied. Total serum IgE levels were measured by a solid phase fluorescent assay and lymphocyte phenotypes were measured by monoclonal antibodies. On multiple linear regression analysis, HIV infection (P=.01) and advanced HIV disease (P < or =.01) were independently associated with increased serum IgE levels, controlling for gender, race, age, and use of injection drugs. In both HIV-seronegative and seropositive individuals, female gender was independently associated with lower IgE levels (P < or = .001). We did not find an independent effect of race or injection drug use on IgE levels. Increased serum IgE levels were associated with HIV infection, the highest levels existing in those with advanced HIV disease. Women had lower IgE levels than men, independent of HIV status. Active or past drug use, race, and age were not found to be independently associated with serum IgE levels. Further studies are necessary to elucidate the mechanisms underlying the increased serum IgE levels seen with HIV infection and its associated immunodeficiency, and to substantiate and explore the decreased levels found in women.

Effect of prior hepatitis B infection on serum IgE levels in patients with human immunodeficiency virus infection.

Advanced HIV infection is associated with increased serum IgE levels, which in turn have been associated with a poor prognosis. Our preliminary data revealed that serum IgE levels were significantly elevated in HIV seropositive injection drug users compared with HIV seropositive non-injection drug users. Since viral hepatitis is common among injection drug users and is itself associated with elevated serum IgE levels, we studied whether there was an association between increased serum IgE levels and positive hepatitis serology in HIV-seropositive patients. A retrospective cross-sectional analysis was performed. The medical records of ambulatory HIV-infected patients in an ongoing study were reviewed. Forty-five patients had hepatitis A, B, and C serology performed. The associations between serum IgE levels and hepatitis A, B and C antibodies, CD4 and CD8 lymphocyte percentages, injection drug use, and sex were analyzed by univariate and multiple regression analyses. On univariate analyses, hepatitis B antibody was significantly associated with increased serum IgE levels in HIV-infected subjects (P = .013), especially in those with AIDS (P = .015). Multiple regression analyses controlling for CD4 lymphocyte percentages, sex, and drug use, confirmed that hepatitis B antibody status remained significantly associated with increased serum IgE levels (P = .05). There was no association of serum IgE levels with hepatitis A or C serology. Prior hepatitis B infection is significantly associated with increased serum IgE levels in advanced HIV infection. The clinical implications of this finding deserve further study.

Frequency and activity of IgE-secreting peripheral blood B-cells in atopic eczema.

Increased immunoglobulin (Ig) E-levels are frequently found in the sera of patients with atopic eczema. To further understand the mechanisms underlying this increase of IgE, like enlarged number of IgE-producing cells, enhanced activity of IgE-producing cells or altered IgE metabolism, we analyzed the frequency and activity of IgE-producing B-lymphocytes within peripheral blood mononuclear cells of patients with atopic eczema. By use of a sensitive solid phase enzyme-linked immunospot assay (ELISPOT), IgE-secreting cells could be visualized within peripheral blood mononuclear cells of 14 individuals (12 patients with atopic eczema, one patient with impetigo contagiosa, one patient with allergic contact dermatitis) at a frequency of 10-1,120 IgE-secreting cells/10(5) B-lymphocytes. The number of IgE-secreting cells was markedly correlated with the corresponding serum IgE-level (r = 0.97). Secretory activity was also reflected by in vitro IgE production, which was assessed in parallel 7-day cultures and found to be related with actual serum IgE-levels. The enhanced serum IgE-levels in patients with atopic eczema seem to result primarily from an increased number of circulating IgE-secreting B-cells, which may also be found, however, in patients with elevated serum IgE-levels, showing different skin diseases.

Increased IgE-levels in bullous pemphigoid correlate to soluble low affinity Fc-II-receptor for IgE and soluble IL-2-receptor

Background Increased serum-IgE levels in patients with bullous pemphigoid (BP) are one of the well known immunological deviations in this autoimmune dermatosis.Aim and methods Since the mechanism that leads to an increase of IgE in BP is still unclear, we investigated serum-IgE levels and IgE regulating cytokines (soluble low affinity Fc II receptor for IgE, IL-4, IFN-g and soluble IL-2 receptor) in sera and blister fluids of 15 BP patients before and during treatment with immunosuppressants using an ELISA-technique.Results All 15 patients examined proved to have high IgE levels in blister fluids (>100 KU/l) and 13 of the 15 patients had elevated serum-IgE levels. Soluble low affinity Fc II receptor for IgE (sCD23R) was also increased in sera (7.9 ± 2.4 pg/ml) and ten fold higher in blister fluids (76.7 ± 15.3 pg/ml). Investigation of cytokines interfering with IgE production showed significantly increased levels of the soluble IL-2 receptor in sera whereas the concentrations of IL-4 and IFN-g revealed no significant differences compared to controls. In blister fluids we detected all the cytokines investigated. During treatment with immunosuppressants the elevated concentrations of sCD23R and soluble IL-2 receptor were reduced to normal values.Conclusions The results show a direct correlation between IgE levels, sCD23R and soluble IL-2-receptor concentrations and suggest a connection between increased IgE levels and T-cell activation in BP.

Alcoholic liver damage–toxicity, autoimmunity and allergy

Alcoholic liver damage–toxicity, autoimmunity and allergy

Personality characteristics and serum ige level in patients with atopic dermatitis

On the basis of clinical observations it was predicted that patients with atopic dermatitis (AD) differ from patients with chronic obstructive bronchitis (OB) in three personality variables; excitability (EX), inadequate stress coping (CO), and paranoidity (PA). Sixty-one patients with AD and 15 with OB were assessed using standard scales. Systematic comparisons between groups strongly confirmed these hypotheses. It was further assumed that AD patients with clinically relevant serum IgE levels (IgE ⩽ 100 IU/ml) score significantly higher on EX and CO than those with normal serum IgE levels (IgE < 100 IU/ml). In contrast, no significant differences between these subgroups were expected regarding paranoidity (which may be a consequence of the AD patients' cosmetic problems). These assumptions again were supported by the findings of the present study. The results underline the potential importance of assessing personality variables and serum IgE levels in the diagnosis of AD patients.

The relationship of stress with serum IgE level in patients with bronchial asthma.

The relationship of stress perception and frequency of stressors with serum total Ig E level was investigated in 54 outpatients with bronchial asthma. The GARS (global assessment of recent stress) scale and SRRS (social readjustment rating scale) were used to measure the degree of stress perception and frequency of stressors during a one-year period Total serum Ig E was measured by the PRIST method. 56% of the patients were found to have psychosomatic disorders, but there was no significant difference in stress perception and frequency of stressors between psychosomatic and non-psychosomatic groups. A considerable number of patients (63%) rated their symptoms as severe, but no significant correlation was found between severity of symptoms and stress perception. Severity of stress perception and frequency of stressors did not correlate with serum total Ig E level. Multiple regression analysis revealed that female patients were significantly higher in stress perception than male ones, and that chronicity of illness was more likely to increase stress perception. Extrinsic asthmatics had significantly more negative stressors than intrinsic ones. In conclusion, serum Ig E is considered a stable indicator of allergy not influenced by stress. It was also indicated that patients with bronchial asthma were more likely to perceive physical symptoms than psychological stress.

気管支喘息におけるリンパ球機能に関する研究

Cellular immunity in bronchial asthma has become essential for the regulation of various allergic reactions in the asthmatic attack. The function of peripheral blood lymphocytes of asthmatic patients was examined by the concanavalin A (Con A) induced suppressor cell assay. The suppressor activity of lymphocytes in mitogen-induced blastogenesis was shown to be decreased in patints with atopic and intractable asthma in comparison with the normal control. The suppressor activity in mite antigen induced lymphocyte blastogenesis was also decreased in patients with atopic asthma. Furthermore, the decrease of ConA induced suppressor activity correlated with the increase of serum IgE level in patients with atopic asthma.These findings indicate that the decreased suppressor cell activity is part of the mechanism of attack and may play an important role in the pathogenesis of bronchial asthma.

IgG-, IgA-, and IgE-induced release of leukotriene C 4 by monocytes isolated from patients with atopic dermatitis

Purified peripheral blood monocytes isolated from patients with atopic dermatitis (AD) and from nonallergic normal donors were compared for their abilities to release leukotriene C 4 (LTC 4), leukotriene B 4 (LTB 4) and β-glucuronidase in response to challenge with aggregated immunoglobulins or anti-immunoglobulins. The relationship between mediator release and the number of monocytes that formed rosettes with immunoglobulin-coated indicator cells was examined. Patients with AD had twice as many IgA- and three times as many IgE-rosetting monocytes as normal donors (48 ± 12% versus 27 ± 10% and 40 ± 15% versus 14 ± 3%, respectively), and yet the amounts of IgA- and IgE-induced LTC 4 released were similar for both groups. This apparent discrepancy did not result from a decreased capacity for arachidonate metabolism via the C5-lipoxygenase pathway, since stimulation of monocytes from patients and normal donors with the calcium ionophore A23187 induced similar amounts of LTC 4 and LTB 4 release (LTC 4, 3.0 ± 1.7 versus 3.0 ± 1.0 ng/10 6 cells; LTB 4, 5.3 ± 0.7 versus 5.2 ± 0.5 ng/10 6 cells, respectively). In addition, aggregated IgG-induced LTC 4 release by monocytes of both groups was similar, concomitant with an equivalent number of IgG-rosetting cells. Determination of cytophilically bound IgG and IgE by flow cytometry demonstrated that monocytes from atopic patients had more IgG bound than monocytes from normal donors. Similar amounts of IgE were detected on most monocytes from both groups, despite the higher serum IgE levels of patients. However, approximately 3% to 8% of monocytes from atopic but not normal donors stained brightly for IgE, suggesting that relatively large amounts of cytophilic IgE were bound to a small percentage of the patients' monocytes. Challenge of monocytes with anti-IgE or anti-IgG induced release of similar amounts of LTC 4 for both groups, despite the presence of more cytophilic IgG on monocytes from atopic donors. These data indicate that monocytes from patients with AD release LTC 4 and LTB 4 in response to challenge with aggregated IgE or anti-IgE, as well as aggregated IgG, IgA, and anti-IgG. However, under our in vitro conditions, stimulation of patients' monocytes with aggregated IgA or IgE was not associated with increased mediator release, despite higher percentages of IgA- and IgE-rosetting cells compared to normal donors.

Heterogeneity of serum IgE levels in atopic dermatitis

To determine whether serum IgE levels in patients with atopic dermatitis (AD) have a relationship to familial background of atopic respiratory disease (ARD), serum IgE levels were measured in 50 AD patients who had personal history of ARD, 37 AD patients who did not have personal history of ARD but had family history of ARD, and 52 "pure" AD patients who had neither personal nor family history of ARD. The "pure" AD patients showed significantly lower serum IgE levels than AD patients who had personal or family history of ARD. It is suggested that AD patients may be classified into at least two subgroups: those with ARD predisposition who have an enhanced IgE producing potential, and those without ARD predisposition who have a low or not-enhanced ability for IgE production.