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

A longitudinal study of patients undergoing rush hyposensitization by honey-bee or yellow jacket venom revealed significant changes of the immunophenotypes until the optimal dose was reached, and a progressive reversion to pre-treatment values in the following months. The activation markers CD23 on B cells and CD25 (IL-2 receptor) on T and B lymphocytes decreased. Although there was little variation of the major CD4 and CD8 lymphocyte populations, CD45R+ cells increased whilst CDw29+ lymphocytes diminished. This inverse variation was associated with a peak of CD4+ CD45R+ cells with concomitant decrease in CD4+ CDw29+ cells showing an inverse effect of the treatment on the reciprocal subsets of CD4 lymphocytes. This indicates a shift in the suppressor/inducer to helper/inducer cell ratio early during rush hyposensitization which may also suggest reversion into a less mature stage of CD4+ cells, associated with the transition from a highly allergen-reactive state to progressive unresponsiveness.
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PMID:Concomitant augmentation of CD4+ CD45R+ suppressor/inducer subset and diminution of CD4+ CDw29+ helper/inducer subset during rush hyposensitization in hymenoptera venom allergy. 252 35

The low affinity IgE receptors (Fc epsilon RII/CD23) homologous to animal lectins have the unique property of cleaving-off the extracytoplasmic portion as the soluble form (IgE binding factor; IgE-BF). Molecular analysis using Fc epsilon RII/CD23 cDNA proved that Fc epsilon RII is not unique to B lymphocytes but is expressed on a variety of cell lineages including T lymphocytes, macrophages and eosinophils. In these cell types, IL-4 is a general inducer of this molecule while IFN-gamma down-regulates B cell Fc epsilon RII/CD23 and up-regulates Fc epsilon RII/CD23 on macrophage and eosinophil cell lines. As predicted by the expression of Fc epsilon RII/CD23 in some HTLV-1(+) T cell lines, Fc epsilon RII/CD23 proved to be induced on normal peripheral T lymphocytes by IL-4 or IL-2 in the presence of additional permissive signals. As indicated by IL-2-dependent Fc epsilon RII/CD23 induction, there is an interesting bilateral co-regulation between Fc epsilon RII/CD23 and the 55 kDa chain of the IL-2 receptor complex with Tac antigen (IL-2R/p55(Tac]. Triggering of Fc epsilon RII/CD23 resulted in the enhanced expression of IL-2R/p55(Tac), whereas IL-2 enhanced the expression of Fc epsilon RII/CD23 in some systems. It is suggested that the triggering of cell surface Fc epsilon RII/CD23 by natural ligands is effectively buffered by soluble Fc epsilon RII/CD23 (IgE-BF).
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PMID:Low affinity IgE receptors: regulation and functional roles in cell activation. 253 50

The activation state of thymic T and B lymphocytes was phenotypically and functionally explored in patients with Myasthenia Gravis (MG). We detected no phenotypic signs of activation in fresh total thymic lymphocyte suspensions (CD25 expression) while functional signs of activation were reflected by a significantly higher sensitivity to recombinant IL-2 (rIL-2) without any previous stimulation in MG patients as compared to controls. The response to rIL-2 was time-and dose-dependent, was inhibited by a blocking anti-IL-2 receptor antibody, and was associated to an increase of CD25+ T cells. Thymic B-cell populations purified after T cell and macrophage depletion, expressed at variable levels activation markers such as the transferrin receptor, the CD25, 4F2, CD23 and B8.7 Ag, indicating that a marked proportion of them are activated. Moreover, these B-cell populations were spontaneously sensitive to BCGF-12-kD and to a lesser extent to rIL-2, demonstrating that they also exhibit functional signs of activation. The largest proportion of activated B cells and the most intense response to BCGF-12-kD was found in patients presenting the highest anti-acetylcholine receptor (AChR) titers. Our data confirm the hyperactivity of the thymus gland in MG, reflected by the presence of T and B cells with functional signs of pre-activation. These cells could conceivably be located in lymphoid follicles and may represent autoreactive cells involved in the autoimmune process. Whether they are sensitized to AChR remains to be investigated.
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PMID:B- and T-cell activation in the thymus of patients with myasthenia gravis. 262 39

A B cell line derived from a human nodular lymphocytic lymphoma (Brill-Symmers) was shown to be dependent on the presence of a low molecular weight B cell growth factor (BCGF) for its growth in vitro. The caryotype was normal and no contamination with Epstein-Barr virus (EBV) could be detected. These cells did not respond to recombinant gamma interferon or to recombinant human interleukin 2 (IL-2), although they displayed a weak density of IL-2 receptor sites. They were both responsive to and dependent on BCGF for their multiplication in vitro. Furthermore, the putative receptor for this growth factor (CD23) was detected on these cells and the BCGF-dependent proliferation could be blocked by a monoclonal anti-CD23 antibody. A tumour-derived cell line like this provides an interesting model for studying the mechanisms regulating B cell growth and the early events leading to the process of B cell immortalization.
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PMID:A B cell growth factor-dependent cell line derived from a human lymphocytic nodular lymphoma. 311 29

Interleukin-4 (IL-4) has various activities on B cells and on hematopoietic cells. We previously reported that TUGm2, a monoclonal antibody to the gamma subunit of the IL-2 receptor (IL-2R gamma), inhibited IL-4-dependent proliferation of CTLL2, a cytotoxic T cell line. We proposed that IL-2R gamma is required for the functional IL-4 receptor (IL-4R) in T cells. In the present work, we further examined whether or not IL-2R gamma is involved in IL-4R function in mouse myeloid cell lines and splenic B cells. TUGm2 suppressed the IL-4-induced proliferation of BA/F3 or IC2 cells, as well as of purified splenic B cells. TUGm2 partially suppressed proliferation of B cells induced by the combination of IL-4 and anti-immunoglobulin M (IgM) antibody. In contrast, TUGm2 had no effect on proliferation of B cells induced by anti-IgM antibody alone or lipopolysaccharide (LPS). TUGm2 also inhibited IgE production induced by IL-4 of LPS-stimulated B cells. The induction of major histocompatibility complex class II molecules or CD23 by IL-4 was virtually unaffected by TUGm2 antibody. These results indicate that IL-2R gamma is differentially involved in various IL-4-dependent reactions.
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PMID:Involvement of the interleukin-2 receptor gamma subunit in interleukin-4-dependent activation of mouse hematopoietic cells and splenic B cells. 784 21

The present study was designed to quantify the level of the soluble form of ICAM-1 (sICAM-1) produced by mononuclear cells (MNC) of rheumatoid arthritis (RA) patients, and to correlate these levels with the disease activity and with the amounts of cytokines or rheumatoid factors (RF) produced by MNC. Unstimulated synovial fluid (SF) MNC produced higher amounts of sICAM-1 than peripheral blood (PB) MNC in RA patients (P < 0.01). sICAM-1 production by PHA-stimulated MNC was higher in RA SF MNC than RA or normal PB MNC (P < 0.01). The amounts of SICAM-1 produced correlated with the amounts of soluble IL-2 receptor produced (P < 0.02) but not with IL-1B or the Lansbury activity index in RA PB MNC. sICAM-1 correlated with the amounts of soluble CD23 and IL-4 produced by normal PB MNC (P < 0.01). The amounts of sICAM-1 correlated with IgG-RF (P < 0.02) and IgM-RF (P < 0.01) produced by unstimulated MNC obtained from the bone marrow (BM) of RA patients. ICAM-1 expression of T-lymphocyte subsets, B lymphocytes, and monocytes obtained from RA PB and RA BM assayed by two-color flow cytometry ranged from 0.1 to 6%, which was not appreciably different from that of normal controls. The monocyte fraction of RA PB MNC produced significantly higher amounts of sICAM-1 than lymphocyte fraction. These results suggest that sICAM-1 produced by MNC may be a marker of cell activation in T and B lymphocytes, in contrast to the transient increase of ICAM-1 expression.
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PMID:Production of soluble ICAM-1 by mononuclear cells from patients with rheumatoid arthritis patients. 791 53

The regulation of the interleukin-4 receptor (IL-4R) was studied at mRNA and protein level in monocytic cells on stimulation with activators of different intracellular signaling pathways and IL-4. Activation of protein kinase C-dependent pathways with phorbol myristate acetate (PMA) or activation of protein kinase A-dependent pathways with DBcAMP and prostaglandin E2 resulted in an augmented IL-4R expression at mRNA and protein level. Transcriptional and posttranscriptional mechanisms seemed to be involved in the promotive effect of DBcAMP because the transcription rate increased 1.8-fold, and the half-life of IL-4R mRNA was prolonged to 150 minutes compared with 120 minutes in unstimulated cells. In contrast, the effect of PMA could only be ascribed to changes at transcriptional level. However, activation of Ca(2+)-dependent pathways with A23187 or stimulation with IL-4 had no effect on the IL-4R expression. The unresponsiveness to IL-4 could not be ascribed to a nonfunctional receptor because IL-4 did modulate the CD14, CD23, and HLA-DR antigen expression. These results are in contrast with IL-4R regulation in T cells, which is affected by IL-4- and Ca(2+)-dependent pathways. The discrepancy might be caused by the presence of the common IL-2 receptor gamma chain (gamma c) in T cells and the absence of the gamma c in monocytic cells, as has been shown by polymerase chain reaction. These data indicate that IL-4Rs are differentially regulated, depending on the cell type studied.
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PMID:Interleukin-4 receptor regulation in human monocytic cells. 802 87

The cell line described here was established for a 50-year-old male patient with rapidly progressive non-Hodgkin's lymphoma whose marrow was diffusely infiltrated with large granular lymphocytes (LGL). Immunophenotyping of marrow blasts and peripheral lymphocytes was positive for CD56, CD2 and CD7, and negative for CD3. Cytotoxicity of peripheral blood mononuclear cells at an effector: target (E:T) cell ratio of 50:1 was 79% against K562 cells and 48% against Daudi cells. To establish the line, cells from the peripheral blood were placed into enriched alpha medium containing 12.5% fetal calf serum, 12.5% horse serum, 10(-4) M beta-mercaptoethanol and 10(-6) M hydrocortisone. Growth of the line (termed NK-92) is dependent on the presence of recombinant IL-2 and a dose as low as 10 U/ml is sufficient to maintain proliferation. Conversely, cells die within 72 h when deprived of IL-2; IL-7 and IL-12 do not maintain long-term growth, although IL-7 induces short-term proliferation measured by 3H-thymidine incorporation. None of the other cytokines tested (IL-1 alpha, IL-6, TNF-alpha, IFN-alpha, IFN-gamma) supported growth of NK-92 cells which have the following characteristics: surface marker positive for CD2, CD7, CD11a, CD28, CD45, CD54, CD56bright; surface marker negative for CD1, CD3, CD4, CD5, CD8, CD10, CD14, CD16, CD19, CD20, CD23, CD34, HLA-DR. DNA analysis showed germline configuration for T-cell receptor beta and gamma genes. CD25 (p55 IL-2 receptor) is expressed on about 50% of all cells when tested at 100 U/ml of IL-2 and its expression correlates inversely with the IL-2 concentration. The p75 IL-2 receptor is expressed on about half of the cells at low density irrespective of the IL-2 concentration. NK-92 cells kill both K562 and Daudi cells very effectively in a 4 h51-chromium release assay (84 and 86% respectively, at an E:T cell ratio of 5:1). The cell line described here thus displays characteristics of activated NK-cells and could be a valuable tool to study their biology.
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PMID:Characterization of a human cell line (NK-92) with phenotypical and functional characteristics of activated natural killer cells. 815 60

Lymphocyte cultures of persons sensitized to the hemoglobin allergen Chi t I show a highly significant response to the allergen measured in the lymphocyte stimulation assay by (3H)-thymidine uptake. In this study, we investigated by flow cytometry the expression of different cell surface markers on lymphocytes after in vitro stimulation for 7 d with or without the allergen Chi t I. We determined the expression of the low-affinity receptor for IgE (CD23) on lymphocytes of Chi t I-sensitized patients and Chi t I-exposed as well as nonexposed controls. CD23 expression was significantly higher in patients than in nonexposed controls. Exposed but healthy subjects showed intermediate values. We also determined the expression of activation markers CD25 (IL-2 receptor) and HLA-DR on the lymphocytes of patients and nonexposed controls. HLA-DR expression on non-T cells (CD3-) was significantly higher in patients than in controls. HLA-DR on T cells (CD3+), and CD25 as well as CD23 expression, could be significantly enhanced after antigen-specific stimulation in patients but not in controls, whereas alpha/beta-T-cell-receptor expression was significantly reduced in patients. Differences between patients and controls were not observed in response to tetanus toxoid (TT) and phytohemagglutinin (PHA). Our results demonstrate antigen-specific influences on the expression of cell surface molecules. These findings may be valuable diagnostic information.
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PMID:Allergen-induced expression of cell surface markers on lymphocytes of Chi t I-sensitized patients. 819 48

Increased serum IgE and enhanced susceptibility to viral infections, decreased levels of interferons, lymphocytic skin infiltrates and IgE-bearing epidermal Langerhans cells are striking features in patients with atopic eczema (AE). Since the hyper-IgE syndrome is known to improve under alpha-interferon (alpha-IFN) therapy, we treated 7 patients with severe AE and high serum IgE exclusively with 3 x 10(6) units IFN alpha 2b thrice weekly for 3 months. Before treatment the skin infiltrates mainly consisted of CD3+/CD4+/TcR alpha/beta + lymphocytes, whereas the CD3+/CD8+ phenotype was limited to about 10% of cells. After 6 weeks of therapy, epidermal inflammation with CD4+ and CD8+ cells was reduced but dense infiltrates remained in papillary perivascular areas. Expression of TcR gamma/delta, HLA-DR and CD25 showed no significant changes. Initially high serum IgE and soluble CD23 as well as cell-bound IgE dropped under therapy, whereas a short-term elevation in serum IL-2 receptor was observed. On peripheral blood lymphocytes slightly reduced expression of HLA-DR, LFA-1, CD23 and ICAM-1 was seen after 100 days. LFA-3 expression became reduced in 4 patients, the CD4/CD8 ratio decreased in all cases. After an initial therapeutic response of all patients, significant longer-lasting improvement of the skin lesions could only be observed in 2 of 7 patients. The data of our long-term study suggest that systemic IFN alpha 2b treatment leads to a remarkable reduction in epidermal inflammation but does not significantly influence cutaneous cell subsets. Immunomodulatory effects became obvious by reduced peripheral cell subsets expressing TcR alpha/beta, MHC class II and adhesion molecules.
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PMID:Effects of interferon-alpha-2b on the clinical course, inflammatory skin infiltrates and peripheral blood lymphocytes in patients with severe atopic eczema. 849 70


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