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IL-2 Receptor (il-2 + receptor)

Distribution by Scientific Domains
Medical Sciences84%
Life Sciences15%
Distribution within Medical Sciences
Immunology27%
Dermatology17%

Kinds of IL-2 Receptor

  • soluble il-2 receptor
    		•

    Selected Abstracts

    Disengaging the IL-2 Receptor with Daclizumab Enhances IL-7,Mediated Proliferation of CD4+ and CD8+ T Cells

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2009
    P. Monti
    Allograft rejection is mainly driven by the production of IL-2, which expands T cells by linking the IL-2 receptor (IL-2R) composed of three subunits: CD25, CD122 and CD132. Daclizumab, widely used in immunosuppression, is a humanized anti-CD25 antibody that disrupts IL-2 signaling by binding to CD25 and preventing the assembly of the high-affinity IL-2R. Here we show that Daclizumab, while blocking the T-cell response to IL-2, increases CD4+ and CD8+ T-cell proliferative response to the homeostatic cytokine IL-7. The IL-7R shares CD132 with the IL-2R and blocking of CD25 by Daclizumab results in the enhanced formation of the IL-7R that in turn allows IL-7 to bind more efficiently on the cell surface. The consequently increased IL-7R signaling boosts intracellular phosphorylated STAT5 and T-cell proliferation. In addition, treatment with Daclizumab delays the internalization of CD127 upon IL-7 treatment, retaining T-cell sensitivity to IL-7 for a prolonged time. This effect of Daclizumab highlights the redundancy of the cytokine system, which may influence T-cell proliferation in transplanted patients, and provides information to improve future immunosuppressive strategies. [source]

    Role of interleukin-15 in the development of mouse olfactory nerve

    CONGENITAL ANOMALIES, Issue 4 2009
    Tsuyoshi Umehara
    ABSTRACT Interleukin (IL)-15 interacts with components of the IL-2 receptor (R) and exhibits T cell-stimulating activity similar to that of IL-2. In addition, IL-15 is widely expressed in many cell types and tissues, including the central nervous system. We provide evidence of a novel role of IL-15 in olfactory neurogenesis. Both IL-15 and IL-15R, were expressed in neuronal precursor cells of the developing olfactory epithelium in mice. Adult IL-15R, knockout mice had fewer mature olfactory neurons and proliferating cells than wild-type. Our results suggest that IL-15 plays an important role in regulating cell proliferation in olfactory neurogenesis. [source]

    Serum levels of IL-18 and sIL-2R in patients with alopecia areata receiving combined therapy with oral cyclosporine and steroids

    EXPERIMENTAL DERMATOLOGY, Issue 2 2010
    Deborah Lee
    Please cite this paper as: Serum levels of IL-18 and sIL-2R in patients with alopecia areata receiving combined therapy with oral cyclosporine and steroids. Experimental Dermatology 2010; 19: 145,147. Abstract:, This study was to determine which immunologic factors contribute to the prognosis of patients with alopecia areata (AA) who were receiving oral cyclosporine A and methylprednisolone. Patients with >25% hair regrowth were defined as responders, and patients exhibiting ,25% regrowth were poor-responders. The serum levels of IL-18 and soluble IL-2 receptor (sIL-2R) were measured at baseline in 21 patients with AA and 22 control subjects. The mean serum level of IL-18 in the patients with extensive AA was significantly higher than that in the control subjects. The mean serum concentration of sIL-2R in the AA patients significantly decreased after 1 month of treatment. The mean basal serum level of IL-18 was highest in the responder, whereas the baseline level of sIL-2R was significantly higher in the poor-responder group than other groups. In conclusion, increased serum sIL-2R level and lower IL-18 level at baseline was associated with a poor prognosis in patients with AA. [source]

    T cell anergy and costimulation

    IMMUNOLOGICAL REVIEWS, Issue 1 2003
    Leonard J. Appleman
    Summary:, T lymphocytes play a key role in immunity by distinguishing self from nonself peptide antigens and regulating both the cellular and humoral arms of the immune system. Acquired, antigen-specific unresponsiveness is an important mechanism by which T cell responses to antigen are regulated in vivo. Clonal anergy is the term that describes T cell unresponsiveness at the cellular level. Anergic T cells do not proliferate or secrete interleukin (IL)-2 in response to appropriate antigenic stimulation. However, anergic T cells express the IL-2 receptor, and anergy can be broken by exogenous IL-2. Anergy can be induced by submitogenic exposure to peptide antigen in the absence of a costimulatory signal provided by soluble cytokines or by interactions between costimulatory receptors on T cells and counter-receptors on antigen-presenting cells. The molecular events that mediate the induction and maintenance of T cell anergy are the focus of this review. The molecular consequences of CD28,B7 interaction are discussed as a model for the costimulatory signal that leads to T cell activation rather than the induction of anergy. [source]

    Interleukin-4 supports interleukin-12-induced proliferation and interferon-, secretion in human activated lymphoblasts and T helper type 1 cells

    IMMUNOLOGY, Issue 1 2006
    Martin A. Kriegel
    Summary Interleukin-12 (IL-12) and IL-4 are known to differentially promote T helper (Th) cell differentiation. While IL-12 induces interferon-, (IFN-,) production and maturation of Th1 cells, IL-4 is thought to antagonize IL-12 and to favour Th2 development. Here we studied the combined action of various concentrations of common ,-chain (,c -chain) cytokines, including IL-4 and the Th1 cytokine IL-12, in human activated lymphoblasts and Th1 cells. IL-4 and IL-7 potentiated IL-12-induced proliferation at every concentration tested (1,10 ng/ml) without increasing rescue from apoptosis, indicating that proliferation was directly affected by these cytokine combinations. With regards to cytokine secretion, IL-2 together with IL-12 initiated tumour necrosis factor-, synthesis, enhanced IFN-, production, and shedding of soluble IL-2 receptor , as expected. Importantly, combining IL-4 with IL-12 also enhanced IFN-, secretion in lymphoblasts and a Th1 cell line. Investigating signal transduction in lymphoblasts induced by these cytokines, we found that not only IL-2 but also IL-4 enhances signal transducer and activator of transcription 3 (STAT3) tyrosine phosphorylation by IL-12. Tyrosine phosphorylations of janus kinase 2 (JAK-2), tyrosine kinase 2 (TYK2), extracellular signal-regulated kinase (ERK) and STAT4, STAT5 and STAT6 were not potentiated by combinations of these cytokines, suggesting specificity for increased STAT3 phosphorylation. In conclusion, two otherwise antagonizing cytokines co-operate in activated human lymphoblasts and Th1 cells, possibly via STAT3 as a converging signal. These data demonstrate that IL-4 can directly enhance human Th1 cell function independently of its known actions on antigen-presenting cells. These findings should be of importance for the design of cytokine-targeted therapies of human Th-cell-driven diseases. [source]

    Disrupted B-lymphocyte development and survival in interleukin-2-deficient mice

    IMMUNOLOGY, Issue 2 2001
    Michael Schultz
    Summary Interleukin-2-deficient (IL-2,/,) mice develop a spontaneous, progressive, CD4+ T-cell-mediated colitis with an age-related decrease in the number of B lymphocytes. The aim of this study was to determine the mechanisms of B-cell loss in IL-2,/, mice. Serum immunoglobulin G1 (IgG1) levels in 8-week-old IL-2,/, mice were above normal but then decreased dramatically with advancing age. Between 8 and 11 weeks of age, the number of B-cell progenitors (B220+ IgM,) in the bone marrow of IL-2,/, mice was less than half of those in IL-2+/+ littermates. By 22 weeks of age, very few progenitor cells remained in the bone marrow of most mice, and spleens were almost devoid of B cells. Likewise, B1 cells were not present in the peritoneal cavity of aged IL-2,/, mice. Flow cytometry analysis of B-cell differentiation in the bone marrow suggested a progressive loss of B cells from the most mature to the least mature stages, which was not dependent on IL-2 receptor-, (IL-2R,) expression. B cells transferred from normal animals had similar survival rates in IL-2,/, and wild-type mice. We conclude that conventional B cells in older IL-2,/, mice are lost by attrition owing to a derangement in B-cell development. Because B1 cells are less dependent on the bone marrow, a separate mechanism for their loss is suggested. [source]

    Mechanistic study of saikosaponin-d (Ssd) on suppression of murine T lymphocyte activation

    JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2009
    Vincent Kam Wai Wong
    Abstract Saikosaponin-d (Ssd) is a triterpene saponin derived from the medicinal plant, Bupleurum falcatum L. (Umbelliferae). Previous findings showed that Ssd exhibits a variety of pharmacological and immunomodulatory activities including anti-inflammatory, anti-bacterial, anti-viral and anti-cancer effects. In the current study we have investigated the effects of Ssd on activated mouse T lymphocytes through the NF-,B, NF-AT and AP-1 signaling pathways, cytokine secretion, and IL-2 receptor expression. The results demonstrated that Ssd not only suppressed OKT3/CD28-costimulated human T cell proliferation, it also inhibited PMA, PMA/Ionomycin and Con A-induced mouse T cell activation in vitro. The inhibitory effect of Ssd on PMA-induced T cell activation was associated with down-regulation of NF-,B signaling through suppression of IKK and Akt activities. In addition, Ssd suppressed both DNA binding activity and the nuclear translocation of NF-AT and activator protein 1 (AP-1) of the PMA/Ionomycin-stimulated T cells. The cell surface markers like IL-2 receptor (CD25) were also down-regulated together with decreased production of pro-inflammatory cytokines of IL-6, TNF-, and IFN-,. These results indicate that the NF-,B, NF-AT and AP-1 (c-Fos) signaling pathways are involved in the T cell inhibition evoked by Ssd, so it can be a potential candidate for further study in treating T cell-mediated autoimmune conditions. J. Cell. Biochem. 107: 303,315, 2009. © 2009 Wiley-Liss, Inc. [source]

    Daclizumab induction therapy in liver transplant recipients with renal insufficiency

    ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2010
    S. K. Asrani
    Summary Background, The role of interleukin 2 (IL-2) receptor antibodies to avoid the nephrotoxic effects of calcineurin inhibitors in the early post-liver transplant (LT) period is not well defined. Aim, To examine the use of daclizumab induction in LT recipients with renal insufficiency. Methods, Between 2002 and 2005, 62 patients (median pre-LT creatinine 2.4 mg/dL, IQR 1.9,3.7) received daclizumab induction with tacrolimus being administered when serum creatinine was <2.0 mg/dL. A concurrent comparison group (n = 221, 2002,2005) received tacrolimus-based immunosuppression without daclizumab (median pre-LT creatinine 1.1 mg/dL, IQR 0.9,1.4). A second historical comparison group (n = 103, 1995,2005) not receiving daclizumab was matched to the daclizumab patients by pre-LT serum creatinine (2.2 mg/dL, IQR 1.8,3.1). All patients received mycophenolate mofetil and steroids. Results, Serum creatinine improved in the daclizumab group (,1.0 mg/dL, IQR ,2.2 to ,0.4) and worsened in the concurrent comparison group (+0.2 mg/dL, IQR 0,0.5) from pre-LT to 4 months. However, there was no difference when daclizumab group was compared with the historical comparison group matched on pre-LT creatinine (median change: ,0.8 mg/dL vs. ,0.7 mg/dL). Daclizumab induction was not associated with improvement in renal function at 4 months (P = 0.34) after adjusting for pre-LT creatinine, age, gender, hepatitis C status and simultaneous liver kidney transplantation. Conclusion, The incremental benefit offered by induction therapy with IL-2 receptor antibodies to preserve renal function is questionable. [source]

    Relation of bone mineral density with clinical and laboratory parameters in pre-pubertal children with cystic fibrosis

    PEDIATRIC PULMONOLOGY, Issue 7 2009
    Nazan Cobanoglu MD
    Abstract To study bone mineral density (BMD) of pre-pubertal cystic fibrosis (CF) children, and its relation with clinical and laboratory parameters, we enrolled 16 CF (8 girls) (4,8 years), and 16 control children (8 girls) (4,8 years). After anthropometric measurements, BMD, serum calcium, phosphorus, total alkaline phosphatase (ALP), 25-hydroxy vitamin D (25-OHD), parathyroid hormone, osteocalcin, tumor necrosis factor (TNF)-,, soluble TNF-, receptor 2 (sTNFR2), and soluble IL-2 receptor (sIL-2R) levels, and urinary calcium and hydroxyproline excretions were assessed. Disease severity of CF patients was determined with Shwachman,Kulczycki clinical and Brasfield radiological scoring systems. The mean Shwachman,Kulczycki and Brasfield scores of CF patients were indicating well-controlled disease. The anthropometric measurements, mean BMD values, and serum calcium, phosphorus and parathyroid hormone levels were within normal range and similar in both groups. Serum osteocalcin levels were lower, and ALP and 25-OHD levels were higher in CF. Although 24-hr urinary calcium excretions was higher in CF patients, hydroxyproline excretions were similar in both groups. There was no difference between two groups for the serum levels of sIL-2R, TNF-, and sTNFR2. Children with low vertebral z -scores had higher serum sIL-2R levels in both groups, but the same relation could not be shown for TNF-, and sTNFR2. We may speculate that younger, healthier and well-nourished patients with CF may have normal BMD, but the bone disease develop as patients get older because of the other contributing factors. Future well-designed longitudinal studies with large cohorts might show a relation with BMD and cytokines in CF. Pediatr Pulmonol. 2009; 44:706,712. © 2009 Wiley-Liss, Inc. [source]

    Successful use of the anti-CD25 antibody daclizumab in an adult patient with hemophagocytic lymphohistiocytosis

    AMERICAN JOURNAL OF HEMATOLOGY, Issue 9 2008
    Rebecca L. Olin
    Hemophagocytic lymphohistiocytosis (HLH) is a rare and severe inflammatory disorder marked by abnormal cytotoxic T and natural killer cell activity, resulting in impaired clearance of pathogen, excessive cytokine production, and continued immune system activation. Soluble IL-2 receptor (sIL-2R or sCD25) is typically elevated in HLH and can serve as a marker of disease activity, although its role in the pathophysiology of the disease is unclear. Here we present a case of an adult patient with steroid-dependent HLH who was treated successfully with daclizumab, a monoclonal anti-CD25 antibody, allowing successful withdrawal of steroid therapy without an increase in symptoms. Am. J. Hematol., 2008. © 2008 Wiley-Liss, Inc. [source]

    Disengaging the IL-2 Receptor with Daclizumab Enhances IL-7,Mediated Proliferation of CD4+ and CD8+ T Cells

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2009
    P. Monti
    Allograft rejection is mainly driven by the production of IL-2, which expands T cells by linking the IL-2 receptor (IL-2R) composed of three subunits: CD25, CD122 and CD132. Daclizumab, widely used in immunosuppression, is a humanized anti-CD25 antibody that disrupts IL-2 signaling by binding to CD25 and preventing the assembly of the high-affinity IL-2R. Here we show that Daclizumab, while blocking the T-cell response to IL-2, increases CD4+ and CD8+ T-cell proliferative response to the homeostatic cytokine IL-7. The IL-7R shares CD132 with the IL-2R and blocking of CD25 by Daclizumab results in the enhanced formation of the IL-7R that in turn allows IL-7 to bind more efficiently on the cell surface. The consequently increased IL-7R signaling boosts intracellular phosphorylated STAT5 and T-cell proliferation. In addition, treatment with Daclizumab delays the internalization of CD127 upon IL-7 treatment, retaining T-cell sensitivity to IL-7 for a prolonged time. This effect of Daclizumab highlights the redundancy of the cytokine system, which may influence T-cell proliferation in transplanted patients, and provides information to improve future immunosuppressive strategies. [source]

    Vaccination with selected synovial T cells in rheumatoid arthritis

    ARTHRITIS & RHEUMATISM, Issue 2 2007
    Guangjie Chen
    Objective This pilot clinical study was undertaken to investigate the role of T cell vaccination in the induction of regulatory immune responses in patients with rheumatoid arthritis (RA). Methods Autologous synovial T cells were selected for pathologic relevance, rendered inactive by irradiation, and used for vaccination. Fifteen patients received T cell vaccination via 6 subcutaneous inoculations over a period of 12 months. Results T cell vaccination led to induction of CD4+ Tregs and CD8+ cytotoxic T cells specific for T cell vaccine. There was selective expansion of CD4+,V,2+ Tregs that produced interleukin-10 (IL-10) and expressed a high level of transcription factor Foxp3, which coincided with depletion of overexpressed BV14+ T cells in treated patients. CD4+ IL-10,secreting Tregs induced by T cell vaccination were found to react specifically with peptides derived from IL-2 receptor ,-chain. The expression level of Foxp3 in CD4+ T cells and increased inhibitory activity of CD4+,CD25+ Tregs were significantly elevated following T cell vaccination. The observed regulatory immune responses collectively correlated with clinical improvement in treated patients. In an intent-to-treat analysis, a substantial response, defined as meeting the American College of Rheumatology 50% improvement criteria, was shown in 10 of the 15 patients (66.7%) and was accompanied by a marked improvement in RA-related laboratory parameters. Conclusion These findings suggest that T cell vaccination induces regulatory immune responses that are associated with improved clinical and laboratory variables in RA patients. [source]

    Cytokine alterations in lichen sclerosus: an immunohistochemical study

    BRITISH JOURNAL OF DERMATOLOGY, Issue 5 2006
    A.M. Farrell
    Summary Background, Although the histology of lichen sclerosus is characteristic, the precise nature of the inflammatory changes and the signals provoking them is uncertain. Objectives, To delineate the inflammatory changes in lichen sclerosus more accurately by studying cytokine changes. Methods, An immunohistochemical study of 12 specimens of genital lichen sclerosus and one specimen of extragenital lichen sclerosus was undertaken using monoclonal antibodies to interferon (IFN)- ,, IFN- , receptor, tumour necrosis factor (TNF)- ,, interleukin (IL)-1,, IL-2 receptor (CD25), intercellular adhesion molecule-1 (ICAM-1) and its ligand CD11a. Control specimens were seven specimens of normal vulva obtained during gynaecological procedures, three specimens of normal skin, adjacent uninvolved thigh from three of the patients with lichen sclerosus, five specimens of nonvulval psoriasis, four specimens of nonvulval lichen planus and two specimens from chronic wounds. Results, The lichen sclerosus specimens demonstrated slightly increased staining for IFN- , within the epidermis compared with the normal vulva and nonvulval skin. There was increased dermal staining for IFN- , both within the pale zone of the upper dermis and within the inflammatory zone below this. We confirmed our previous demonstration that in lichen sclerosus HLA-DR immunostaining is increased in association with vascular endothelium, the inflammatory cell infiltrate and around the keratinocytes. The areas of the epidermis with the strongest immunostaining for HLA-DR generally also had the strongest staining for IFN- ,. In the lichen sclerosus specimens the zone of inflammation also demonstrated increased immunostaining for TNF- ,, IL-1,, IFN- , receptor, CD25, CD11a and ICAM-1 while the zone of sclerosus demonstrated a smaller increase in immunostaining for IFN- , receptor, TNF- ,, CD11a and ICAM-1, and the epidermis demonstrated increased staining for ICAM-1. Conclusions, The increased staining for IFN- ,, TNF- ,, IL-1,, IFN- , receptor, CD25, CD11a and ICAM-1 suggest that the cytokine response in lichen sclerosus shares characteristics of the cytokine response in lichen planus and chronic wounds. [source]