Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injection of mice with a foreign anti-IgD Ab stimulates B and T cell activation that results in large cytokine and Ab responses. Because most anti-IgD-activated B cells die before they can be stimulated by activated T cells, and because IL-4 prolongs the survival of B cells cultured with anti-Ig, we hypothesized that treatment with IL-4 at the time of anti-IgD Ab injection would decrease B cell death and enhance anti-IgD-induced Ab responses. Instead, IL-4 treatment before or along with anti-IgD Ab suppressed IgE and IgG1 responses, whereas IL-4 injected after anti-IgD enhanced IgE responses. The suppressive effect of early IL-4 treatment on the Ab response to anti-IgD was associated with a rapid, short-lived increase in IFN-gamma gene expression but decreased CD4+ T cell activation and decreased or delayed T cell production of other cytokines. We examined the possibilities that IL-4 stimulation of IFN-gamma production, suppression of IL-1 or IL-2 production, or induction of TNF-alpha or Fas-mediated apoptosis could account for IL-4's suppressive effect. The suppressive effect of IL-4 was not reversed by IL-1, IL-2, or anti-TNF-alpha or anti-IFN-gamma mAb treatment, or mimicked by treatment with anti-IL-2Ralpha (CD25) and anti-IL-2Rbeta (CD122) mAbs. Early IL-4 treatment failed to inhibit anti-IgD-induced Ab production in Fas-defective lpr mice; however, the poor responsiveness of lpr mice to anti-IgD made this result difficult to interpret. These observations indicate that exposure to IL-4, while T cells are first being activated by Ag presentation, can inhibit T cells activation or promote deletion of responding CD4+ T cells.
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PMID:IL-4 suppression of in vivo T cell activation and antibody production. 1065 18

A 31-year-old man had received corticosteroids for 20 months for treatment of a brain tumor, and his blood eosinophil count ranged from 100/microliter to 1,000/microliter. On June 24th, 1998, he was re-admitted because of dyspnea secondary to left massive pleural effusion. Peripheral blood examination revealed an eosinophil count of 48,000/microliter. The eosinophils were hypersegmented, with abnormal distribution of eosinophilic granules and formation of cytoplasmic vacuoles. Blasts and basophils were not increased, hemoglobin was 13.4 g/dl, and the platelet count was 79,000/microliter. Bone marrow was slightly hypercellular with 55% eosinophils and 0.2% blasts. The patient's karyotype was normal, and Wilms' tumor gene was not detected. Serum IgE was normal and serum vitamin B12 and soluble IL-2 receptor were elevated. Serum levels of eosinophilopoietic cytokines, IL-3, IL-5, and GM-CSF, were low. Specimens of pleural fluid contained many eosinophils. Because the eosinophil count increased to 110,000/microliter on July 2nd, hydroxyurea was started without effect. On July 16th, the eosinophil count reached 167,000/microliter, and vincristine was added. The eosinophil count rose to 253,000/microliter the next day, and cytarabine and daunorubicin were administered, but the patient died of septic shock. Although the clinical course suggested eosinophilic leukemia, monoclonal proliferation of eosinophils was not demonstrated. To our knowledge, this is the highest peripheral blood eosinophil count reported in the literature to date.
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PMID:[Rapidly progressive, refractory eosinophilia with a 250,000/microliter eosinophil count]. 1072 43

The house dust mite Dermatophagoides pteronyssinus allergen Der p 1 elicits IgE antibody responses in a significant proportion of patients suffering from dust mite allergy. We have recently shown that Der p 1 proteolytically cleaves a cell surface molecule involved in the homeostatic control of human IgE synthesis, namely the IL-2 receptor (CD25) on T cells. As a result, these T cells show markedly diminished proliferation and IFN-gamma secretion in response to stimulation by anti-CD3 antibody. However, these observations still leave open the important issue of whether CD25 cleavage, and the consequent suppression of IFN-gamma secretion, leads to enhanced IL-4 secretion, and whether such cytokine changes would be exhibited by both CD4 and CD8 T cells. Here we demonstrate for the first time that the proteolytic activity of Der p 1 biases human CD4 and CD8 T cells towards a type 2 cytokine profile. Our data provide compelling evidence for the role of the proteolytic activity of Der p 1 in creating a microenvironment conducive for IgE synthesis.
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PMID:Human T cell subset commitment determined by the intrinsic property of antigen: the proteolytic activity of the major mite allergen Der p 1 conditions T cells to produce more IL-4 and less IFN-gamma. 1129 46

Elevated IgE responses and eosinophilia observed in patients with atopic dermatitis (AD) may reflect increased responses of type 2 T-helper (Th2) cytokines with a concomitant decrease in interferon-gamma (IFN-gamma) production. However, the cross-regulation of Th1/Th2 derivation and function in AD patients are incompletely characterized. Therefore, we investigated serum levels of several cytokines [interleukin (IL)-18, IL-12, IL-10, IL-2 and IFN-gamma] in patients with AD to assess their possible relationships to the severity of disease. Serum IL-18 levels in AD patients were significantly higher than those in healthy controls [207 pg/mL; 95% confidence interval (CI), 172-242 pg/mL vs. 144 pg/mL; 95% CI, 116-178 pg/mL; P = 0.026]. Those IL-18 levels significantly correlated with eosinophil counts and serum soluble IL-2 receptor (sIL-2R) levels, and showed a tendency to correlate with clinical severity scores and serum IgE levels. IL-2 levels showed a significantly inverse correlation with serum IgE levels, and IL-12 levels clearly correlated with IL-10 levels. These results suggest the value of serum IL-18 levels as a parameter of AD activity and may support a possible role for IL-18 in the pathogenesis of AD. The inverse correlation between IgE levels and IL-2 levels suggests that IgE production may be inhibited by IL-2 in patients with AD. Furthermore, the correlation of IL-12 levels with IL-10 levels may support the previous reports that show the induction of IL-10 production by human natural killer cells and/or T cells stimulated with IL-12 in vitro.
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PMID:Serum cytokine levels in atopic dermatitis. 1207 14

Immunological parameters were studied in 45 patients with active tuberculous spondylitis, admitted for surgical treatment, who were divided into 2 groups in accordance with the prevalence of exudative-necrotic, or productive components of inflammation in the vertebral bodies and paravertebral tissues. The patients with a predominantly exudative-necrotic component of inflammation exhibited a severe clinical course with frequent neurological disorders, large abscesses in the paravertebral tissues, inflammatory changes in the leukogram, enhanced specific T-lymphocytic activity in the PPD blast-transformation reaction, significant increases in the levels of tuberculosis antibodies and IgE, IL-2 and it soluble IL-2 receptor RR-alpha, an excessively high increase in the functional activity of neutrophilic granulocytes, and lower with IgG2. The degree of immunological disorders corresponds to the severity of a course of tuberculous spondylitis.
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PMID:[Immunity in patients with active tuberculous spondylitis]. 1291 37

Because abnormalities in redox balance cluster in type I diabetes families and the intracellular thiol redox status seems to modulate immune function, we aimed to investigate the relationship between oxidative stress and immunological features. We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low-affinity IgE receptor, and CD25 or IL-2 receptor) from 38 type I patients, 76 low-risk (i.e. without underlying islet autoimmunity) non-diabetic first-degree relatives of diabetic patients, and 95 healthy subjects. In type I diabetes families, protein and lipid oxidation was confirmed by the presence of reduced sulphhydryl groups, increased advanced oxidation protein products, and increased plasma and erythrocyte malondialdehyde. Relatives had decreased counts of monocytes, of cells co-expressing CD23 and CD25 and of CD25(+) cells in peripheral blood. Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4(+)CD8(+) lymphocytes and increased serum levels of soluble receptors for interleukin (IL)-6 and IL-2. Abnormal indicators of oxidative stress were related in part to immune abnormalities. In the whole study group, we found a correlation (multiple R 0.5, P < 0.001) of CD23(+)CD25(+) cells with blood counts of monocytes, CD4(+)CD8(+) cells, CD25(+) cells, basal haemolysis and plasma levels of thiols. In type I diabetics, anti-GAD65 antibody levels were associated (multiple R 0.6, P = 0.01) positively with sIL-6R, negatively with duration of diabetes and CD23(+)CD25(+) counts; plasma creatinine correlated positively (multiple R 0.6, P < 0.001) with both sIL-2R and tumour necrosis factor (TNF)-alpha concentration. Our study reports the first evidence that the oxidative stress observed in type I families is related to immunological hallmarks (decreased peripheral numbers of monocytes as well as cells bearing a CD4(+)CD8(+), CD23(+)CD25(+) and CD25(+) phenotype) from which the involvement of some immunoregulatory mechanisms could be suspected. It remains to be elucidated the course of events culminating in the loss of physiological immune homeostasis and disease pathology.
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PMID:Redox status and immune function in type I diabetes families. 1514 59

Severe atopic dermatitis causes major impairment in the life of both children and their parents. Generally, symptoms can be controlled with emollients, topical steroids, antibiotics, antihistaminic but some patients remain intensely ill and may require treatment with systemic steroids and so on. Cyclosporin has been found to be effective in a variety of inflammatory skin disorders since it reduces the number of activated T-cells expressing interleukin 2 (IL-2) receptors. In order to monitor the safety and clinical efficacy of therapy and days of remission we performed Cyclosporin on 3 children with severe atopic dermatitis, refractory to all traditional therapies. Cyclosporin suspension at dosage of 5 mg/kg daily, in 2 doses for 8 weeks has been used. Cyclosporin blood levels, liver and kidney function, blood pressure and some immunological parameters (eosinophils, IgE, IL-2 receptors) were monitored. All patients showed a marked clinical improvement with reduction of pruritus, erythema, papules, vesciculation, excoriation, scaly crusts and lichenification. No clinical or haematological side effects were demonstrated. The soluble IL-2 receptor concentration decreased even after 8 weeks of treatment in all 3 patients, regardless of IgE levels (case 1: low IgE level; case 2: very high IgE level) as in several others T-cell mediated non IgE-related skin disease. The authors suggest that courses of 8 weeks seem effective and safe as well as longer time in producing early remission with the advantage of a low cumulative exposure to the drug. The main question is whether a prolonged remission will permain as well as continuous therapy. This study underscores the potential value of systemic administration of this powerful immuno-suppressive agent in the treatment of many cases of severe atopic dermatitis working regardless of the IgE values. Although 3 cases report does not justify any definitive conclusion however it does a contribute to understand the heterogeneity of atopic dermatitis and it adds information to its current treatment guidelines.
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PMID:Cyclosporin is safe and effective in severe atopic dermatitis of childhood. Report of three cases. 1524 10

Drug-induced hypersensitivity syndrome (DIHS) is a rare but severe disease with multiorgan failure. Recently, the association of the human herpesvirus (HHV) family, particularly of HHV-6, with DIHS has been reported. We report a 43-year-old female diagnosed as having DIHS based on the clinical course and laboratory examinations. The HHV-6 reactivation was demonstrated by significantly increased levels of the specific antibody in her paired sera and by polymerase chain reaction of HHV-6 DNA. Notably, transient hypogammaglobulinaemia was detected in the early stage of the disease, which was associated with the disease activity. By contrast, the serum IgE level and eosinophils were increased 2 or 3 weeks later. In addition, serum levels of interferon gamma, interleukin (IL)-4 and soluble IL-2 receptor, which were increased in the early phase of the disease, decreased gradually after the corticosteroid therapy.
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PMID:Drug-induced hypersensitivity syndrome associated with transient hypogammaglobulinaemia and increase in serum IgE level. 1594 27

The present report is a case control study aimed to determine the levels of cytokines and other parameters in the sera of allergy-complicated and uncomplicated giardiasic children before and after metronidazole treatment. The study included a total of 126 subjects; 52 giardiasic children, 34 allergy-complicated giardiasis (36.9%) and 34 healthy controls, as well as six cases of giardiasis simultaneously infected with other parasites or bacterial pathogens. Serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, soluble IL-2 receptor (sIL-2R), IL-6, IL-8, nitric oxide (NO), and C-reactive protein (CRP) were determined. TNF-alpha and sIL-2R levels significantly increased in giardiasic cases. IL-1beta, IL-6, IL-8, CRP, and NO levels increased only in the cases associated with allergy. All increased variables significantly decreased following metronidazole treatment and returned to normal levels. Metronidazole-treated patients became 100% parasite free. In conclusion, increased TNF-alpha and sIL-2R may be involved in pathogenesis of non-allergic giardiasis and probably Th1 type immune response seems to be predominant and this response may be protective rather than causative of the disease. Activation of the immune system takes place in giardiasis. It is broader and more intense in allergy-complicated giardiasis than that of uncomplicated cases, most probably due to non-invasive character of G. lamblia. Enhanced IgE production pointed to Th2-type immune response and confirms its association with allergy.
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PMID:Serum cytokine changes in Turkish children infected with Giardia lamblia with and without allergy: Effect of metronidazole treatment. 1597 46

Airway pathologies have been comprehensively researched in adult asthma, but in children, the extent of airway inflammation associated with episodic wheeze, often diagnosed as asthma, has not been fully characterized. It is not clear whether persistent airway inflammation is present in the absence of wheezing symptoms, and there is controversy regarding the role of age and atopy. This study assessed cellular and cytokine markers of airway inflammation in asymptomatic children with a history of episodic wheeze. Children with a history of episodic wheeze and cough (study group) and nonasthmatic patients requiring elective surgery (control group) were recruited. All subjects in the study group had a history of significant episodic wheezing (>2 episodes per year), and used only as-needed beta-agonist treatment. Bronchoalveolar lavage (BAL) was obtained using bronchoscopic lavage (study group) and nonbronchoscopic lavage (control group). Differential cell counts of BAL and flow cytometry were performed to identify T-lymphocyte phenotypes, and intracellular cytokine profiles were measured after phorbol-12-myristate 13-acetate (PMA) stimulation of BAL fluid T-cells. Twenty-one children with a history of 2-12 episodes of wheeze per year and 21 nonasthmatic subjects without respiratory symptoms were recruited. Study and control subjects were matched for age (median age, 5 years) and demographic characteristics. Study subjects had higher IgE levels, but their measurements were still within normal range. No significant differences in BAL differential cell counts were noted, and in both groups, the majority of T-cells were CD3+ CD8+, with a median CD4:CD8 ratio of 0.6. There was no significant difference in T-cell expression of the activation markers HLA-DR and CD25 (IL-2 receptor), or in PMA-induced production of the intracellular cytokines IFN-gamma, IL-2, IL-4, IL-5, and IL-10. The results of this study suggest that significant T-cell-driven airway inflammation is absent in mild or nonatopic, asymptomatic children of this age group who have episodic wheeze. Our findings support asthma management guidelines that do not recommend long-term treatment of this group of patients with anti-inflammatory medications.
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PMID:Airway inflammation in asymptomatic children with episodic wheeze. 1661 54


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