Increased FcepsilonR1alpha expression with upregulated CD203c expression on peripheral basophils is seen in patients with chronic urticaria (CU). However, there has been no published report on the association between CD203c expression level and clinical disease activity in CU patients. To investigate whether the increase of basophil activation is associated with the disease activity of CU, we measured basophil CD203c expression using a tricolor flow cytometric method in 82 CU patients and 21 normal controls. The relationship between the percentage of CD203c-expressing basophils and clinical parameters was analyzed. The mean basophil CD203c expression was significantly higher in CU patients than in healthy controls (57.5% vs 11.6%, P < 0.001). The basophil CD203c expression in severe CU patients was significantly higher than in non-severe CU (66.5% +/- 23.3% vs 54.0% +/- 23.3%, P = 0.033). Multiple logistic regression analysis indicated that both > or = 72% basophil CD203c expression and urticaria activity score (UAS)> or = 13 were significant predictors of severe CU (P = 0.005 and P = 0.032, respectively). These findings suggest that the quantification of basophil activation with CD203c at baseline may be used as a potential predictor of severe CU requiring another treatment option beyond antihistamines.
Adult ; Autoantibodies/blood ; Basophils/*immunology ; Female ; Flow Cytometry ; Humans ; Immunoglobulin E/blood/immunology ; Male ; Phosphoric Diester Hydrolases/biosynthesis/*immunology ; Pyrophosphatases/biosynthesis/*immunology ; Receptors, IgE/biosynthesis ; Urticaria/*immunology

Childhood minimal change nephrotic syndrome (MCNS) has often been associated with allergic symptoms such as urticaria, bronchial asthma, atopic dermatitis, allergic rhinitis and elevated IgE levels and referred to involve immune dysfunction. Fc epsilon RII is known to be involved in IgE production and response. Interleukin-4 is being recognized as a major cytokine up-regulating IgE production. Hence the present study is aimed at investigating the role of interleukin-4 and Fc epsilon RII in the pathogenesis of MCNS. IgE was measured by ELISA. Fc epsilon RII was analyzed by fluorescence activated cell scanner (FAC-scan) by double antibody staining with anti Leu16-FITC and anti Leu20-PE. Soluble IgE receptor was measured by ELISA using anti CD23 antibody (3-5-14). Interleukin-4 activities were measured by CD23 expression on purified human tonsillar B cells. Serum IgE levels were significantly higher in MCNS (1,507 +/- 680 IU/dl) than in normal controls (123 +/- 99.2 IU/dl). A significantly higher expression of membrane Fc epsilon RII was noted for MCNS (41 +/- 12%) than that in normal controls (18 +/- 6.2%) (p < 0.001). Soluble CD23 levels were also significantly higher in MCNS (198 +/- 39.3%) than in normal controls (153 +/- 13.4) (p < 0.01). Interleukin-4 activity in sera of MCNS (12U/ml) was also significantly higher than normal controls (4.5U/ml). These results indicate that increased production of Fc epsilon RII and interleukin-4 may play an important role in the pathogenesis of MCNS.
B-Lymphocytes/immunology ; Child ; Humans ; Immunoglobulin E/blood ; Interleukin-4/*physiology ; Nephrosis, Lipoid/*etiology/physiopathology ; Receptors, IgE/biosynthesis/*physiology ; Solubility

OBJECTIVES AND METHODS: To confirm the local production of IgE antibody from the nasal polyp tissue, and to evaluate the difference between atopics and non-atopics, nasal polyp tissues were taken from both 10 atopic and 10 non-atopic subjects. The tissue total IgE (tlgE) level was measured by enzyme-linked immunosorbent assay (ELISA) and serum tlgE level by radio-immunoassay. The tissue albumin level was measured by nephelometry, and serum albumin level by Bromocresol green method. RESULTS: The polyp tissue tlgE/albumin as well as serum tlgE/albumin ratio were significantly higher in atopics than in non-atopics (p < 0.05), with no difference in the albumin level between the two groups (p > 0.05). Three non-atopic subjects had high polyp tissue tlgE/albumin (> 10). A significant correlation was noted between serum tlgE/albumin and polyp tlgE/albumin (r = 0.46, p = 0.04). The ratio of polyp tlgE/albumin to serum tlgE/albumin was greater than 1 in all of the non-atopic subjects and 7 of 10 atopic subjects. CONCLUSION: These findings support the hypothesis that IgE antibody could be locally produced from the nasal polyp tissue of non-atopic subjects as well as atopic subjects. The possibility of an isolated local production of IgE antibody was suggested.
Albumins/analysis ; Antibodies, Anti-Idiotypic/analysis* ; Biopsy, Needle ; Comparative Study ; Enzyme-Linked Immunosorbent Assay ; Female ; Human ; Hypersensitivity, Immediate/immunology* ; IgE/biosynthesis* ; IgE/analysis ; Male ; Nasal Polyps/pathology ; Nasal Polyps/immunology* ; Radioimmunoassay ; Reference Values ; Tissue Culture ; Substances: IgE ; Substances: Antibodies, Anti-Idiotypic ; Substances: Albumins

The prevalence studies on specific IgE to toluene diisocyanate (TDI)-human serum albumin (HSA) conjugate in TDI-induced asthma have shown variable results. In this study, we attempted to compare specific IgE bindings to TDI-HSA conjugate and its specificity using 3 different conjugates. Sera were collected from 20 TDI-induced asthma and 10 controls. Specific IgE were measured by ELISA using three TDI-HSA conjugates; two from Carnegie Mellon (CM; 98 and 99 CM conjugates) and one from Ajou University. To evaluate specificity and cross-reactivity, ELISA inhibition tests were applied. Positive and negative predictive values between Ajou conjugate and 98 CM conjugate were 75% and 100%. Those between Ajou and 99 CM were 100% and 93.8%. One patient showed an isolated positive response to the Ajou with negative responses to the other two conjugates. ELISA inhibition test using this patient's serum revealed the significant inhibitions by the Ajou and minimal inhibitions by the others. On the other hand, another patient showed an isolated positive response to 99 CM with negative responses to the others, and ELISA inhibition test showed significant inhibition by 99 CM with minimal inhibitions by the others. These results suggest that specific IgE bindings to a new antigenic determinant of TDI-HSA conjugate can be heterogeneous and differ from one individual to another.
Asthma/immunology ; Asthma/chemically induced* ; Enzyme-Linked Immunosorbent Assay ; Human ; IgE/biosynthesis* ; Serum Albumin/immunology* ; Toluene 2,4-Diisocyanate/immunology* ; Toluene 2,4-Diisocyanate/adverse effects

For those with allergy, vaccination with a specific allergen has often been used as a major therapeutic measure. However, the universal application of this technique in clinics have been restricted due to its low success rates and the risk of active systemic anaphylactic shock (ASAS). In this regard, we constructed a fusion protein (OVA-DT), ovalbumin (OVA) fused with diphtheria toxin protein (DT), which may exert a specific cytotoxicity to cells bearing OVA-specific IgE. Its therapeutic effect was evaluated in mice (BALB/c) sensitized with OVA (Os-mice). OVA challenges to the OVA-sensitized mice (Os-mice) caused ASAS to death within 30 min, but OVA-DT treatment afforded mice complete protection. When OVA-DT was treated to the Os-mice, none showed the signs of ASAS when re-challenged 48 h after the treatment. OVA-DT itself was not found to be toxic or allergenic in normal mice. The effect of OVA-DT on the biological functions of mast cells was also studied. Binding of OVA-DT to OVA-specific IgE bearing mast cells and the inhibition of histamine release from these cells were observed. In addition, OVA-DT treatment inhibited the proliferation of OVA-specific B cells in mice. In Os-mice treated with OVA-DT, levels of anti-OVA IgG2a in serum and the production of IFN-gamma by splenic lymphocytes were found to increase, but the production of IL-4 by these cells decreased. Re-direction of cytokine profiles from OVA-specific Th2 to OVA-specific Thl is suggested. These results indicate that OVA-DT can protect Os-mice from ASAS due to OVA challenge, because it inactivates OVA-specific IgE-expressing cells, including mast cells and B cells.
Anaphylaxis/prevention | control* ; Animal ; B-Lymphocytes/immunology ; Female ; Histamine Release/drug effects ; IgE/metabolism ; Interferon Type II/biosynthesis ; Interleukin-4/biosynthesis ; Lymphocyte Transformation/drug effects ; Mast Cells/metabolism ; Mice ; Mice, Inbred BALB C ; Ovalbumin/immunology* ; Recombinant Fusion Proteins/therapeutic use*