No abstract available.
Interleukin-2* ; Interleukins* ; Mucocutaneous Lymph Node Syndrome* ; Receptors, Interleukin-2*

BACKGROUND: Interleukin-2 receptor (IL-2) is expressed and released predominantly activated T lymphocyte. Increased serum levels of soluble IL-2R have been noted in a variety of autoimmune diseases and in conditions associated with T lymphocyte activation. OBJECTIVE: We aimed to examine whether the T lymphocyte activation has any association with the pathogenesis of Behçet's disease. METHOD: We have measured the serum level of soluble IL-2R in serum samples obtained from 67 patients with Behçet's disease and 30 healthy people as a control group, using a double-antibody sandwich enzyme-linked immunosorbent assay technique. RESULTS: Serum soluble IL-2R levels were found to be significantly elevated in the group of Behçet's disease as compared with the control group. No significant differences were found within clinical subtypes of Behçet's disease. CONCLUSION: These findings suggest the presence of an ongoing T lymphocyte activation in this disease process.
Autoimmune Diseases ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-2* ; Lymphocyte Activation ; Lymphocytes ; Methods ; Receptors, Interleukin-2*

BACKGROUND: Interleukin-2 receptor (IL-2) is expressed and released predominantly activated T lymphocyte. Increased serum levels of soluble IL-2R have been noted in a variety of autoimmune diseases and in conditions associated with T lymphocyte activation. OBJECTIVE: We aimed to examine whether the T lymphocyte activation has any association with the pathogenesis of Behçet's disease. METHOD: We have measured the serum level of soluble IL-2R in serum samples obtained from 67 patients with Behçet's disease and 30 healthy people as a control group, using a double-antibody sandwich enzyme-linked immunosorbent assay technique. RESULTS: Serum soluble IL-2R levels were found to be significantly elevated in the group of Behçet's disease as compared with the control group. No significant differences were found within clinical subtypes of Behçet's disease. CONCLUSION: These findings suggest the presence of an ongoing T lymphocyte activation in this disease process.
Autoimmune Diseases ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-2* ; Lymphocyte Activation ; Lymphocytes ; Methods ; Receptors, Interleukin-2*

Culture of human peripheral T lymphocytes with irnmobilized anti-CD3 rnAb plus IL-2 resulted in a marked proliferation and the enhancing IL-2Ra mRNA expression. The process of the T cell activation involves a series of biochemical events which ultimately lead to the proliferation and IL-2Ra mRNA expression. Although the above results have been observed, the celluar signal mechanisms between the proliferative response and the IL-2Ra mRNA expression through T cell receptor and IL-2 receptor remains unresolved. In the present study, We have used genistein (the selective PTK inhibitor) or chronic PMA treatment (depletion of intracelluar PKC activity), to investigate the role of PTK or PKC both in a synergistic proliferation and in the enhancing IL-2Ra mRNA expression by IL-2/anti-CD3. Genistein (30 ug/ml) completely blocked IL-2 induced T cell proliferation, and inhibited anti-CD3 induced T cell proliferation (93.4%). But genistein downregulated the IL-2Ra mRNA expression by IL-2, anti-CD3 and IL-2/anti-CD3. The chronic PMA treatment failed to inhibit the proliferation and the IL-2R#u mRNA expression by IL-2 alone. But PKC depleted T cells stimulated with anti-CD3 mAb showed the decrease of the proliferation (68.6%) and IL-2Ra mRNA expression. In activated with IL-2/anti- CD3, the proliferative response showed a half of reduction, but the IL-2Ra mRNA expression were not regulated. These results demonstrate that proliferative response to IL-2 appears to be dependent on PTKs activity and independent of PKC involvement, but the IL-2Ra mRNA expression may be required another signals. PTKs and PKC activity may be important in TCR/CD3 signaling. But IL-2/anti-CD3 are coupled up different signal transduction pathways responsible for the synergistic T cell proliferation and the enhancing IL-2Ru mRNA expression.
Cell Proliferation ; Genistein ; Humans ; Interleukin-2* ; Receptors, Antigen, T-Cell ; Receptors, Interleukin-2 ; RNA, Messenger* ; Signal Transduction ; T-Lymphocytes

BACKGROUND: Interleukin-5 (IL-5) is responsible for eosinophilia in allergic diseases. In allergic bronchial asthma, there is a correlation between the extent of eosinophil infiltration in bronchial mucosa and IL-5 concentrations. In addition, IL-2 concentration is elevated in the airways and associated with eosinophilia in symptomatic patients with bronchial asthma. In animal studies, IL-2 can induce eosinophilia by increasing the synthesis of IL-5, however, it is still unknown how IL-2 can induce eosinophila in human being. The aim of this study is to evaluation the effect and mechanism of IL-2 on prolongation of eosinophil survival. METHODS: After purifiing the eosinophils from the venous blood of allergic patients with eosinophilia, we measured the survival rates of eosinophils using trypan blue dye exclusion test, and the number of eosinophils with Randolp's solution. We compared the survival rates of eosinophils in the presence of IL-2 or IL-5. Neutralizing antibody for IL-5 was added in IL-2 treated eosinophils to reveal whether IL-2 induced prolongation of eosinophil survival was mediated by IL-5. We checked IL-5 m-RNA expression of lymphocytes in the presence of IL-2 by using Reverse transcription-Polymerase chain reaction (RT-PCR) method to revealed the effect of IL-2 on IL-5 m-RNA expression on lymphocyte. alpha and beta IL-2 receptors were measured on eosinophils and lymphocytes with flow-cytometer after stimulated with IL-2. RESULTS: 1) Eosinophil survival rates increased dose dependently on IL-5 and IL-2. 2) The eosinophil survival rates increased by IL-2 were not inhibited by the pretreatment with neutralizing antibody for IL-5. 3) IL-5 m-RNA was not expressed on lymphocytes by the treatment with IL-2 up to 96 hours. 4) IL-2 upregulate the expression of IL-2Ralpha on eosinophils, instead of no effect on the expression of IL-2Rbeta. CONCLUSION: Interleukin-2 had the enhancing effect on the survival rates of eosinophils. The mechanism behind IL-2 induced eosinophilia might be the increment of IL-2 receptors on eosinophils rather than IL-5 synthesis by lymphocytes.
Animals ; Antibodies, Neutralizing ; Asthma ; Eosinophilia ; Eosinophils* ; Humans ; Interleukin-2 ; Interleukin-2 Receptor alpha Subunit ; Interleukin-5 ; Lymphocytes ; Mucous Membrane ; Receptors, Interleukin-2 ; Survival Rate ; Trypan Blue

OBJECTIVE: Schizophrenia is a disabling disorder of unknown aetiology, lacking definite diagnostic method and cure. A reliable biological marker of schizophrenia is highly demanded, for which traceable immune mediators in blood could be promising candidates. We aimed to gather the best findings of neuroinflammatory markers for first-episode psychosis (FEP). METHODS: We performed an extensive narrative review of online literature on inflammation-related markers found in human FEP patients only. RESULTS: Changes to cytokine levels have been increasingly reported in schizophrenia. The peripheral levels of IL-1 (or its receptor antagonist), soluble IL-2 receptor, IL-4, IL-6, IL-8, and TNF-α have been frequently reported as increased in FEP, in a suggestive continuum from high-risk stages for psychosis. Microglia and astrocytes establish the link between this immune signalling and the synthesis of noxious tryptophan catabolism products, that cause structural damage and directly hamper normal neurotransmission. Amongst these, only 3-hydroxykynurenine has been consistently described in the blood of FEP patients. CONCLUSION: Peripheral molecules stemming from brain inflammation might provide insightful biomarkers of schizophrenia, as early as FEP or even prodromal phases, although more time- and clinically-adjusted studies are essential for their validation.
Astrocytes ; Biomarkers ; Encephalitis ; Humans ; Interleukin-1 ; Interleukin-4 ; Interleukin-6 ; Interleukin-8 ; Metabolism ; Methods ; Microglia ; Polytetrafluoroethylene ; Psychotic Disorders ; Receptors, Interleukin-2 ; Schizophrenia ; Synaptic Transmission ; Tryptophan

Interleukin-5 (IL-5), which is known to be an activator of human eosinophil, increases in IgA nephropathy. In order to find out the relationship between activated eosinophil function and the pathogenesis of Henoch-Sch nlein purpura (HSP) and IgA nephropathy, serum esosinophil cationic protein (ECP) was analyzed using a monoclonal antibody Besides, the soluble IL-2 receptor (sIL-2R) was analyzed to clarify if there was a positive correlation between T cells and activated eosinophils. As anticipated, the levels of ECP, in detail, were significantly higher among HSP patients with a mean of 9.7+/-1.8microgram/L than in a control group with a mean of 4.6+/-0.7microgram/L. The HSP patients were also classified as one group with normal urine and another group with abnormal urine. The latter showed higher levels of ECP than the former. On the other hand, the levels of ECP were higher in IgA nephropathy patients than in the control group; however, there was no significance in statistics. The sIL-2R levels were higher in HSP patients than those in serums of IgA nephropathy patients and the control group. Thus, this study came to a conclusion that the activated eosinophil might be one of the pathogeneses in HSP but not in IgA nephropathy.
Eosinophil Cationic Protein* ; Eosinophils* ; Glomerulonephritis, IGA* ; Hand ; Humans ; Immunoglobulin A* ; Interleukin-5 ; Purpura ; Receptors, Interleukin-2 ; T-Lymphocytes

OBJECTIVE: To investigate the clinical value of expression level of interleukin-2 receptor (IL-2R) and interleukin-8 (IL-8) in the fever patients with hematological malignancies. METHODS: A total of 121 inpatients in the First Affiliated Hospital of Anhui Medical University from April 2018 to October 2019 were enrolled in this study. The patients were separated into infection group (61 cases) and non-infection group (60 cases). In the meantime, 40 healthy people without fever or infection in the hospital for physical examination were set as matched group. C-reactive protein (CRP), procalcitonin (PCT), and cytokines were detected in all the patients with fever after admission and infection control. While, blood samples were taken from healthy people during physical examination. RESULTS: The expression levels of IL-2R in infection group were higher than those in the control group (P<0.001), and the level of serum IL-2R in infection group was also higher than that in the non-infection group (P<0.05). Based on Spearman analysis, in patients with malignant hematologic disease, serum IL-2R level was positively correlated with CRP (r=0.557, P<0.001) and IL-8 (r=0.479, P<0.001), and IL-8 level was positively correlated with CRP (r=0.318, P<0.001). Compared with the non-infection group, the area under the curve (AUC) for the level of CRP, PCT, and IL-2R of the infection group was 0.714 (95%CI: 0.623-0.806), 0.765 (95%CI: 0.680-0.851), and 0.761 (95%CI: 0.686-0.836), the sensitivity was 0.705, 0.852, and 0.705, and the specificity was 0.717, 0.70, and 0.60, respectively. While, AUC of CRP+PCT, CRP+IL-2R, PCT+IL-2R, and CRP+PCT+IL-2R was 0.789 (95%CI: 0.712-0.866), 0.702 (95%CI: 0.623-0.782), 0.757 (95%CI: 0.677-0.838), and 0.789 (95%CI: 0.712-0.866), the sensitivity was 0.738, 0.934, 0.705, and 0.738, and the specificity was 0.840, 0.470, 0.810, and 0.840, respectively. CONCLUSION CRP, PCT, IL-2R, and IL-8 are useful parameters for diagnosis of the infectious fever in patients with hematological malignancies, which provides the basis of initial diagnosis and rational use of antibioties for clinician.
Biomarkers ; C-Reactive Protein ; Calcitonin ; Calcitonin Gene-Related Peptide ; Hematologic Neoplasms ; Humans ; Interleukin-8 ; Protein Precursors ; Receptors, Interleukin-2 ; Sepsis

BACKGROUND: Cough Coughing is the most common complaint for which patients seek medical service. When cough sustains caughing continues over 3 weeks in non-smokers who do not take cough-provoking drugs, they are classified as patients with chronic cough. As well-known, three Three well known main causes of chronic caugh are diseases - (delete) postnasal drip syndrome, bronchial asthma and gastroesophaseal reflux disease. - comprise the majority of the causes of chronic cough. Among them, postnasal drip syndrome is reported to be the most common cause of all in chronic cough diseases, and allergic inflammation plays an important role in the pathogenesis of postnasal drip syndrome. CD23 and CD25 which are low affinity receptor for IgE and IL-2 receptor alpha, respectively, are closely related to allergic inflammation and we evaluated the role of them in their roles were evaluated in chronic cough patients. METHODS: We evaluated 105 patients with chronic cough and selected 56 patients for measurement of serum CD23 & CD25 level levels. We selected 10 normal, medical students for comparison of serum CD23 & CD25 level. levels. RESULT: We found that postnasal drip syndrome was The postnasal drip syndrome was found to be the most common cause of chronic cough. Serum CD23 and CD25 level were did not increased increase in chronic cough patient compared to normal controls. However in bronchial asthma patient, serum CD23 level was increased relative to normal control (p<0.05). CONCLUSION: In bronchial asthma presented as chronic cough, lymphocyte mediated allergic inflammation might be may related with the pathogenesis of the disease.
Asthma ; Cough* ; Humans ; Immunoglobulin E ; Inflammation ; Lymphocytes ; Receptors, Interleukin-2 ; Students, Medical

PURPOSE: The pathogenesis of atopic dermatitis is not clearly defined yet, but the pathogenetic role of Th2 cells has been supposed. CD30 is a membrane-bound glycoprotein that may be expressed on activated T cells with a sustained expression in Th2 cells and can be released as a soluble form(sCD30). This study was done to document the changes of serum sCD30 and it's clinical significance in atopic dermatitis. METHODS: We analyzed serum sCD30, serum soluble IL-2 receptor (sIL-2R), total serum IgE and total eosinophil counts from 18 children with atopic dermatitis(AD), 15 atopic asthmatics without AD (AA), 15 atopic asthmatics with AD(AD+AA), and 14 healthy non atopics(control). We investigated the correlation of serum sCD30 levels with disease severity assessed by clinical scoring(SCORAD index) in the group of AD and AD+AA. RESULTS: The serum levels of sCD30 were significantly higher in the group of AD and AD+AA than the group of AA and control. There were no differences in serum sCD30 levels between the group of AA and control and between the group of AD and AD+AA. The serum sIL-2R levels showed no significant differences among the four groups. There was significant positive correlation between serum sCD30 and serum sIL-2R levels(P<0.05). Both serum sCD30 and serum sIL-2R levels showed no correlation with total serum IgE, total eosinophil counts, and disease severity, respectively. CONCLUSION: Serum sCD30 is elevated only in atopic dermatitis irrespective of presence of asthma. The results suggest that Th2 immune responses may involved the pathogenesis of atopic dermatitis and sCD30 may be the possible marker of atopic dermatitis.
Asthma ; Child* ; Dermatitis, Atopic* ; Eosinophils ; Glycoproteins ; Humans ; Immunoglobulin E ; Receptors, Interleukin-2 ; T-Lymphocytes ; Th2 Cells