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)

Interleukin-2 (IL-2) production as well as the response of lymphocytes to exogenous IL-2 was measured in asymptomatic homosexuals, patients with acquired immune deficiency syndrome (AIDS), and homosexuals with prodromal symptoms. IL-2 production following lectin stimulation was not significantly different in homosexuals compared to age matched heterosexual controls. In contrast, the response of lymphocytes to exogenous IL-2 was significantly decreased in AIDS and homosexuals with prodromal symptoms compared to asymptomatic homosexuals and heterosexual controls. These data, combined with the data of others, suggest that an underlying immune defect in AIDS is abnormal IL-2 receptor expression and resultant poor IL-2 response.
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PMID:Abnormal lymphocyte response to exogenous interleukin-2 in homosexuals with acquired immune deficiency syndrome (AIDS) and AIDS related complex (ARC). 392 51

Interleukin-2 (IL-2) is a T-cell-derived polypeptide hormone of 133 amino acids which exerts its growth-promoting activity via a surface receptor. Originally, IL-2 was believed to be a unique growth factor for activated T cells; more recent studies, however, have demonstrated that certain B-cell tumours as well as normal activated B lymphocytes express a surface molecule which is recognized by monoclonal antibodies directed against the IL-2 receptor. Furthermore, we and others have shown recently that activated B cells proliferate in response to either immunoaffinity-purified or recombinant IL-2. These controversial findings prompted us to undertake a detailed quantitative comparison of IL-2 receptor expression on activated B and T cells. We show here, using biosynthetically labelled IL-2(3H-IL-2) and anti-IL-2 receptor antibody (3H-PC61) that activated B and T cells express both high-affinity (apparent dissociation constant, Kd approximately 20 pM) and low-affinity (Kd approximately 1,000 pM) IL-2 receptors. Binding of IL-2 to both classes of receptor is inhibited by the monoclonal anti-IL-2 receptor antibody PC61. B blasts express half as many total IL-2 binding sites or PC61 binding sites as T blasts, and the ratio of the number of low- to high-affinity receptors for each cell type is approximately 10:1. Immunoprecipitation analysis of surface-labelled blasts indicates that B and T cells have IL-2 receptors of similar relative molecular mass. Taken together, these data suggest strongly that IL-2 can act as a growth hormone for both B and T lymphocytes.
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PMID:Similarities between interleukin-2 receptor number and affinity on activated B and T lymphocytes. 392 47

Interleukin-2 (IL-2) is a lymphokine synthesized by some T cells following activation. Resting T cells do not express IL-2 receptors but receptors are rapidly expressed on T cells following the interaction of antigens, mitogens, or monoclonal antibodies with the antigen specific T-cell receptor complex. Using anti-Tac a monoclonal antibody that recognizes the IL-2 receptor, the receptor has been purified. The receptor is a 33 kdalton peptide that is post-translationally glycosylated to a 55 kdalton mature form. Mature receptors contain both N-linked and O-linked sugars and are both sulfated and phosphorylated. Using an oligonucleotide probe, based on the N-terminal amino acid sequence, cDNAs encoding this receptor have been cloned, sequenced and expressed. The addition of anti-Tac to in vitro culture systems blocks the IL-2 induced DNA synthesis of IL-2 dependent T-cell lines and inhibits soluble auto- and alloantigen induced T-cell proliferation. Furthermore, it prevents the generation of cytotoxic and suppressor effector T cells. The anti-receptor antibody also inhibits lectin stimulated immunoglobulin synthesis and the sequential expression of late appearing activation antigens on T cells. Normal resting T cells and most leukemic T-cell populations do not express IL-2 receptors however the leukemic cells of all patients with human T-cell leukemia/lymphoma virus (HTLV-I) associated, adult T-cell leukemia (ATL) examined expressed the Tac antigen. In HTLV-I infected cells the 42 kdalton long open reading frame (LOR) protein encoded in part, by the pX region of HTLV-I may act as a transacting transcriptional activator that induces transcription of the IL-2 receptor gene thus providing an explanation for the constant association of HTLV-I infection of lymphoid cells and IL-2 receptor expression. The constant display of large numbers of IL-2 receptors which may be aberrant in the ATL cells may play a role in the uncontrolled growth of these leukemic T cells. Patients with the Tac positive ATL are being treated with an anti-Tac monoclonal antibody directed towards this growth factor receptor.
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PMID:Interleukin-2 receptor expression in retrovirus associated adult T-cell leukemia. 610 Jun 44

Interleukin-2 (IL-2) signaling results in tyrosine phosphorylation of the 75-kDa IL-2 receptor (IL-2R) beta chain and the activation of phosphatidylinositol 3'-kinase (PI3-K). Herein, we demonstrate that the 85-kDa (p85) regulatory subunit of PI3-K physically associates with the tyrosine-phosphorylated IL-2R beta chain. A fusion protein containing both the amino- and the carboxyl-terminal src homology 2 domains of p85 precipitates an 80-kDa tyrosine-phosphorylated protein (pp80) from the lysates of IL-2-stimulated, but not unstimulated, human T lymphoblasts. Preclearing studies and immunoblotting with an antiserum to the IL-2R beta chain demonstrates that pp80 represents a portion of the IL-2R beta chain pool. A tyrosine-phosphorylated oligopeptide corresponding to tyrosine 392 of the IL-2R beta chain partially inhibits binding of the IL-2R beta chain by p85 fusion protein, raising the possibility that this residue plays a role in the interaction of PI3-K with the receptor.
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PMID:SH2-dependent association of phosphatidylinositol 3'-kinase 85-kDa regulatory subunit with the interleukin-2 receptor beta chain. 750 94

Delta-9-tetrahydrocannabinol (THC), the major psychoactive component in marijuana, has been shown to suppress a variety of interleukin-2-(IL-2)-dependent cellular functions in both murine and human lymphocytes. These effects were examined in both human peripheral blood lymphocytes (hPBL) and the IL-2-dependent murine cytotoxic T-cell line CTLL-2. Interleukin-2-induced thymidine uptake and uridine uptake were suppressed in a dose related manner when cells were co-incubated for 48 h with 100 U rhIL-2/ml and 1-10 micrograms THC/ml. Interleukin-2-induced protein synthesis was also suppressed in a dose related manner over this THC concentration range, with the hPBL being more susceptible to the suppressive effect of THC than the CTLL-2 cells. Autoradiographic analysis of the synthesized proteins from hPBL cell lysates reveals a generalized suppression of all nascent proteins in THC-treated cultures. Human natural killer cell activity is only affected at the highest concentration tested (10 micrograms THC/ml) while lymphokine-(IL-2)-activated natural killer cell activity is affected throughout the range of 1-10 micrograms THC/ml. Together these results suggest that THC interferes with the IL-2:IL-2 receptor signaling cascade at one or possibly many points causing a decrease in IL-2-induced metabolic activity and cytolytic function.
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PMID:Delta-9-tetrahydrocannabinol treatment results in a suppression of interleukin-2-induced cellular activities in human and murine lymphocytes. 752 19

Variable immunobiological changes occur with alcohol consumption. Previous studies have shown that acetaldehyde forms stable adducts with serum proteins, including albumin. These adducts are elevated in persons and animals consuming ethanol. We examined the effect of serum protein-acetaldehyde adducts formed with fetal bovine serum (FBS) on concanavalin A-stimulated murine splenocytes. Interleukin-2 (IL-2) secretion and IL-2 receptor (IL-2R) expression were determined as a function of the effect of the acetaldehyde-protein adduct(s). FBS was incubated with acetaldehyde (500, 100, 50, 25, 10, and 0 microM) for 1 hr at 37 degrees C. Excess acetaldehyde was removed by ultrafiltration using a 500 molecular weight cut-off membrane in 3 volumes. Free as well as bound acetaldehyde was quantified using fluorigenic HPLC before and after incubation. Recovered acetaldehyde correlated with the amount added (r2 = 0.996). Splenocytes were cultured for 48 hr in complete medium containing 5% acetaldehyde-treated and 5% untreated FBS with 4 micrograms/ml concanavalin A. Although cell viability was unchanged, acetaldehyde-treated FBS mixed with native FBS decreased IL-2 secretion in a dose-dependent manner. The percentage of cells expressing IL-2R was reduced only at the highest acetaldehyde-FBS dose. Therefore, immunological effects ascribed to ethanol may result in part from the toxic properties of acetaldehyde-protein adducts on IL-2 secretion.
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PMID:Acetaldehyde-serum protein adducts inhibit interleukin-2 secretion in concanavalin A-stimulated murine splenocytes: a potential common pathway for ethanol-induced immunomodulation. 762 67

Interleukin-2 (IL-2)-dependent large granular lymphocytes (LGL) with a distinctive surface phenotype were generated from histologically normal duodenal biopsy tissues. Immunoperoxidase staining of the mucosa with an anti-CD56 monoclonal antibody revealed LGL localized in the lamina propria rather than in the epithelium. Light and electron microscopy demonstrated azurophilic and electron-dense cytoplasmic granules. Flow cytometry analysis revealed that these cells express CD45, CD56, CD2, CD7, CD11a, CD18, CD69 and the intermediate affinity (p70) IL-2 receptor (IL-2R) but not CD57, CD16, CD3, CD4, CD5, CD8, CD45RA, CD25, or the high affinity p55 IL-2R. The LGL proliferated when cultured in the presence of human rIL-2 but not in the presence of human rIL-4. Functional studies demonstrated that the LGL had strong cytotoxicity against natural killer (NK) target cells, K562, but not NK-resistant targets such as Colo 205, Melanoma and Epstein-Barr virus (EBV)-transformed B-cell lines. The LGL expressed genes for IL-5, IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumour necrosis factor-alpha (TNF-alpha) and the corresponding cytokines were detected in culture supernatant. These results provide evidence for an important role of gut mucosal LGL in the induction and regulation of inflammation and immunity in the gut.
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PMID:Morphological, phenotypic and functional characteristics of a pure population of CD56+ CD16- CD3- large granular lymphocytes generated from human duodenal mucosa. 769 28

Interleukin-2 (IL-2)-induced generation of non-major histocompatibility complex (MHC)-restricted killer cells among human cord blood lymphocytes (CBL) was investigated. After 1 week in culture with recombinant (r)IL-2 and human serum (HuSer), the cytotoxicity of CBL against K562 and COLO cells greatly exceeded the cytotoxicity of cultured adult peripheral blood lymphocytes. Culturing of CBL with rIL-2 and HuSer led to preferable generation of CD56+ cells. After 1 month in culture, the number and frequency of CD56+ cells had increased by more than 50 and nine times, respectively. The generation of CD56+ cells in CBL cultures may at least partially be explained by their comparatively strong expression of the IL-2 receptor (IL-2R) beta-chain (p75).
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PMID:Non-major histocompatibility complex-restricted killer cells in human cord blood: generation and cytotoxic activity in recombinant interleukin-2-supplemented cultures. 769 29

Interleukin-2 (IL-2) has various trophic and neuromodulatory actions in the mammalian central nervous system (CNS). The interleukin-2 receptor alpha (IL-2R alpha) is an accessory subunit of the IL-2 receptor heterotrimer complex which is essential for 'high' affinity IL-2 binding. Although an IL-2R alpha (or IL-2R alpha-like) epitope has been localized in brain by immunohistocytochemistry, it was unknown whether the IL-2R alpha subunit expressed in brain was derived from the same or a different gene than the lymphocyte IL-2R alpha. Therefore, in the present study, the cDNA comprising the full length coding region was cloned and sequenced from saline-perfused forebrain. The brain IL-2R alpha cDNA was found to be 100% homologous with the corresponding lymphocyte IL-2R alpha cDNA sequence. IL-2R alpha mRNA was expressed at very low levels in saline-perfused forebrain of non-challenged BALB/c mice as well as in saline-perfused forebrain from severe combined immunodeficiency (SCID) mice. The present data, demonstrating IL-2R alpha gene expression in both well-perfused normal and SCID mouse forebrain from which no CD3 gamma gene expression was detected by PCR, provides evidence that the IL-2R alpha clones isolated are from resident brain cells and not from blood lymphocytes (e.g. T lymphocytes). Thus, these findings demonstrate that the protein coding sequence of the mouse brain IL-2R alpha is derived from the same gene coding sequence as the lymphocyte IL-2R alpha, and indicate that previously reported differences in the size of their respective mRNA transcripts appear to be due to differences in untranslated regions.
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PMID:Molecular cloning of the coding sequence of an interleukin-2 receptor alpha subunit cDNA in murine brain. 779 14

The antitumor activity of Interleukin-1 (IL-1), was assessed against the murine adenocarcinoma colon 26 tumor model in combination with Interleukin-2 (IL-2). Colon 26 tumor cells were inoculated on the back of syngeneic BALB/c mice. Fourteen days after inoculation, when the tumor nodule reached approximately 10 mm in diameter, tumor nodules were resected and Hank's solution, IL-2, IL-1, or IL-2 plus IL-1 were injected directly into the mouse spleen. One week after treatment, potent natural killer (NK) and enhanced lymphokine activated killer (LAK) cell activities were seen in the splenocytes treated by the combination of IL-2 plus IL-1. Furthermore the combination treatment by IL-2 plus IL-1 resulted in a significantly prolonged survival. Phenotypic analysis showed an increased number of percent positive cells expressing asialo GM 1 and IL-2 receptor after treatment with IL-2 plus IL-1. A possible role of IL-1 in augmentation of IL-2 dependent antitumor activity in vivo is discussed.
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PMID:Enhanced activity against syngeneic murine tumors by intrasplenic injection of recombinant interleukin-2 (IL-2) and interleukin-1 (IL-1). 780 73


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