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)

During the past few decades intravenous immunoglobulin (IVIG) has been used successfully in the treatment of various immunoregulatory disorders. Treatment results have been attributed to immunomodulation mainly via Fc receptors or by anti-idiotypic antibodies to disease-causing autoantibodies. From the present study it is clearly evident that 7S IVIG (intact immunoglobulin) as well as 5S IVIG [F(ab')2 fragments] and Fc fragments have a potent immunomodulatory capacity. We demonstrate that mainly 7S IVIG inhibits alloantigen-induced T-cell proliferation and generation of cytotoxic T lymphocytes. Reduced interleukin-2 (IL-2) protein levels in culture supernatants of IVIG-supplemented mixed lymphocyte reactions (MLR) but unchanged IL-2 mRNA levels strongly argue in favour of a post-transcriptional interference of IVIG with cytokines and/or cytokine production. Interferon-gamma (IFN-gamma), soluble IL-2 receptor (sIL-2R) and monokines such as IL-1 beta, IL-6, IFN-alpha and tumour necrosis factor (TNF-alpha) were not affected by IVIG supplementation to MLR. Fc fragments were superior to F(ab')2-containing IVIG (5S and 7S IVIG) in inhibiting lectin stimulation of peripheral blood mononuclear cells (PBMC), whereas natural killer (NK) cytotoxicity was primarily inhibited by Fc-bearing IVIG (7S IVIG and Fc fragments), suggesting multiple mechanisms of IVIG immunomodulatory activity.
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PMID:A comparative study of the in vitro immunomodulatory activity of human intact immunoglobulin (7S IVIG), F(ab')2 fragments (5S IVIG) and Fc fragments. Evidence for post-transcriptional IL-2 modulation. 913 49

Fifteen athletes were investigated 24 h before, 1 h after, and 20 h after an exhaustive exercise stress test (mean duration 68 min). Testing for cytokines was done in serum, urine, and the supernatants of whole blood cell cultures, which were stimulated with lipopolysaccharide (LPS), concanavalin A (Con A), or phythaemagglutinin (PHA). Elevated levels of interleukin 6 (IL-6) and soluble IL-2 receptor (sIL-2R) were found 1 h after the run in both serum and urine samples. TNF-alpha in serum was also increased, whereas IL-2 in urine was decreased after the exercise. All other testings in serum and urine (including IFN-gamma) gave borderline or negative results. In cell cultures, the LPS-induced release of the inflammatory cytokines TNF-alpha, IL-1, and IL-6 was suppressed 1 h after exercise. Also, the Con-A-induced and LPS-induced release of IFN-gamma, and the PHA-induced release of IL-2 were suppressed 1 h after exercise. In contrast, Con-A-induced release of IL-2 was mildly increased after the run. We conclude that exercise of the intensity and duration described here causes an activation of the immune system, which is immediately counter-regulated. Twenty hours after the exercise, most of the observed changes were back to pre-exercise levels, indicating only a short duration for this suppressive counter-regulation.
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PMID:Effect of exhaustive exercise stress on the cytokine response. 913 73

Cytokine gene expression was examined by qualitative and semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) in the lungs of Mycoplasma pneumoniae infected immune C57BL/6 mice depleted of either CD4+, CD8+ or both CD4+ and CD8+ T cells. Immediately after M. pneumoniae reinfection of control immune mice, mRNAs for TNF-alpha, IFN-gamma, IL-1 beta, IL-6, IL-2 and IL-2 receptor were promptly detected in the lungs. In animals depleted of CD4+ T cells, mRNA expression for IL-2, IL-2 receptor and IFN-gamma were completely abrogated and mRNA expression for TNF-alpha, IL-1 beta and IL-6 were reduced by 10- to 100-fold. In mice depleted of CD8+ T cells, mRNA expression for IL-2 and the IL-2 receptor was also undetectable, while mRNA for TNF-alpha, IL-1 beta and IL-6 were only marginally decreased. Histological evaluation of the infected lungs performed in parallel revealed dense mononuclear infiltrations around small bronchi and small blood vessels in control reinfected mice. In contrast, in CD4+ T cell-depleted mice, these focal accumulation of lung tissue infiltrating cells were found to be greatly reduced. The data indicate that the inflammatory response in lung tissue thought to be mainly responsible for Mycoplasma pneumoniae disease is associated with an increased level and a prolonged expression of proinflammatory cytokines due to CD4+ lung infiltrating T cells.
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PMID:Cytokine gene expression in immune mice reinfected with Mycoplasma pneumoniae: the role of T cell subsets in aggravating the inflammatory response. 914 34

The goal of this study was to determine the relationship between plasma human immunodeficiency virus (HIV) load and cytokine expression. HIV-RNA plasma levels were determined in 34 HIV-seropositive (HIV+) asymptomatic subjects [range: 0.5 to 211 kiloequivalents (kEq)/ml HIV-RNAJ, by a modified branched-DNA (bDNA) assay. Plasma HIV-RNA levels were positively correlated with increased plasma levels of TNF-alpha, soluble TNF receptor type II, soluble IL-2 receptor, beta 2-microglobulin, and neopterin, but not with plasma IL-6 levels. In contrast, increased viral load and diminished CD4 counts correlated weakly. TNF-alpha mRNA levels, as determined by bDNA technology, were not significantly increased in peripheral blood mononuclear cells (PBMC) isolated from HIV-infected subjects, compared to HIV-seronegative (HIV-) subjects, and were not correlated with plasma levels of HIV-RNA, cytokines, or activation markers. These results are consistent with the hypothesis that a self-reinforcing mechanism exists between TNF-alpha production and generalized immune activation on one hand with HIV replication on the other.
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PMID:Relationship of plasma HIV-RNA levels and levels of TNF-alpha and immune activation products in HIV infection. 919 82

Mercury induces a systemic autoimmune condition characterized by auto-antibodies to the nucleolar protein fibrillarin (AFA) and systemic immune-complex (IC) deposits in genetically susceptible mouse strains. This study examines T cell activation and cytokine production following mercury exposure in genetically susceptible and resistant strains. Mercury injected s.c., according to the protocol for induction of autoimmunity, caused an early T cell activation, measured as an increase of IL-2-producing cells, and increased expression of the IL-2-receptor proteins CD25 and CD122 and of the proliferation marker CD71 on days 2-4 in the susceptible A.SW and A. TH strains. This was followed by a long-lasting increase in the number of T cells, dominated by CD4(+) cells. Mice of the susceptible A.SW strain showed a modest increase of TNF-alpha-, IFN-gamma-, and IL-4-producing cells after 4-6 days, and a very distinct increase of IL-4-producing cells on days 8-10. The susceptible SJL strain (H-2(s)), severely deficient in Th2-promoting CD4(+), NK1.1(+) T cells, showed no increase of IL-4(+) cells on days 8-10. Instead, the number of IFN-gamma-producing cells was increased. Susceptible mice developed an increase of Ig-producing cells, AFA, and systemic IC-deposits. Genetically mercury-resistant A.TL mice showed a minimal increase of T cells, but no increase in cytokine-producing cells. We conclude that autoimmunogenic doses of HgCl2 induce an activation and proliferation of T cells in genetically susceptible mouse strains, as well as a broad increase of cytokine-producing cells, followed by a late predominance of the Th2-associated IL-4. One strain, severely deficient in Th2-promoting CD4(+), NK1.1(+) T cells, lacked the increase in IL-4(+) cells, indicating that a predominantly Th2-response is not necessary for induction of autoimmunity by mercury. However, a Th2-dominated response led to a faster and stronger B cell activation.
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PMID:Effects of the murine genotype on T cell activation and cytokine production in murine mercury-induced autoimmunity. 923 98

NK cells, a key component of the innate immune system, are known to play an important role against viral infections. Previously, we reported that the human herpesvirus-6 (HHV-6) induces IL-15 in human PBMC and increases their NK activity. We describe in this work that another human herpesvirus, HHV-7, which shares genomic homology with HHV-6, also causes up-regulation of NK cell cytotoxicity via IL-15 induction. The NK cell activity of the PBMC from different donors displayed a variable range of enhancement after treatment with HHV-7. This enhancement occurred within a few hours of exposure to the virus and was blocked by Abs to IL-15, but not to other cytotoxicity-enhancing cytokines (i.e., to IFN-gamma, IL-2, TNF-alpha, or IL-12). Our results also show that this HHV-7-induced IL-15-mediated activation of NK cells occurs via IL-2R, since HHV-7-enhanced NK cytotoxic activity could be blocked completely by anti-IL-2R beta-chain mAb (anti-CD122). The up-regulation of NK cell cytotoxicity did not require infectious virus, as the use of UV-irradiated HHV-7 produced similar results. This effect was virus specific because it was abrogated by neutralizing the virus with human sera containing Abs to HHV-7. We also found increased amount of IL-15 transcripts in HHV-7-treated PBMC as compared with the untreated PBMC. Taken together, these results would suggest that host responds to HHV-7 infection by up-regulating IL-15 production, which then results in an enhancement of NK cell activity; this, in turn, may play a major role in the control of the viral infection.
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PMID:Enhancement of natural killer cell cytotoxicity by the human herpesvirus-7 via IL-15 induction. 936 23

In murine acute viral myocarditis, natural killer (NK) cells infiltrate the heart first, followed by activated T-cells, which play an important role in the pathogenesis of the myocardial damage. Because of their multipotential effects, cytokines are thought to play a role in the induction and development of these immune processes. To clarify in more detail the precise mechanism of the cytokine networks involved, the expression of various cytokine mRNAs has been investigated in myocardial cells infected with Coxsackievirus B3 (CVB3) in vivo and in vitro by a semiquantitative polymerase chain reaction (PCR) method. Interleukin (IL)-1 alpha, IL-1 beta, IL-6, tumour necrosis factor (TNF)-alpha, and TNF-beta were expressed almost throughout the early phase of virus infection with some variations. IL-2, IL-3, IL-4, IL-10, interferon (IFN)-gamma, granulocyte/macrophage colony stimulating factor (GM-CSF), and IL-2 receptor (IL-2R) were mainly expressed by the infiltrating cells. TNF-alpha, TNF-beta, and IL-1 beta were also expressed partly by the infiltrating cells. T-helper (Th)1-related cytokines (IL-2, IFN-gamma, and TNF-beta) were more strongly expressed than Th2-related cytokines (IL-4 and IL-10) in vivo, indicating that the Th cells which infiltrated the heart and mediated the immune responses in the early phase of acute myocarditis were mainly of Th1-type.
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PMID:Expression of cytokine mRNAs in murine hearts with acute myocarditis caused by coxsackievirus b3. 937 Sep 55

Follicular dendritic cells (FDCs) in the lymphoid follicle (LF) are essential to the sequential processes of B-cell proliferation, selection, and differentiation. Although the importance of some cytokines in these processes has been pointed out, there is little information about the follicular localization of their receptors. We investigated, with special reference to FDCs, the localization of cytokine receptors as well as cytokines themselves in human tonsils by several means, including immunochemistry, immunoelectron microscopy, reverse transcriptase polymerase chain reaction, and in situ hybridization. FDCs in the follicular apical light zone expressed transforming growth factor-beta receptor II (TGF-betaR II), granulocyte-macrophage colony-stimulating factor receptor alpha (GM-CSFRalpha; CDw116), tumor necrosis factor receptor I (TNFR I; CD120a), interleukin-1 receptor II (IL-1R II; CDw121b), IL-2 receptor beta (IL-2Rbeta; CD122), IL-4 receptor (IL-4R; CDw124), and IL-6 receptor (IL-6R; CD126), among the 10 receptors examined. Those in the basal light zone expressed strongly TNFR I and weakly GM-CSFR alpha, IL-1R II, IL-2Rbeta, IL-4R, and IL-6R, and often those in the outer and mantle zones expressed GM-CSFR alpha, IL-4R, and IL-6R. FDCs in the apical light zone expressed only TGF-beta among the 7 cytokines examined. On the other hand, follicular lymphocytes mainly in the light zone expressed 9 kinds of receptors, with the exception being TGF-betaR II; expression was rather frequent for TNF-alpha, IL-1alpha, and IL-2 and less frequent for TGF-beta, GM-CSF, IL-4, and IL-6. These data indicate that only FDCs mainly in the light zone express many cytokine receptors, although FDCs may produce the cytokine, TGF-beta. Cytokines may act not only on some follicular lymphocytes but also on most FDCs in the light zone expressing cytokine receptors.
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PMID:Expression of cytokine receptors on follicular dendritic cells. 938

Even though blood transfusion-associated immunomodulatory effects have been reported, the basic immune mechanism is still not understood. Data from studies on the clinical effects of allogeneic blood-induced immunosuppression are contradictory. However, there are indications that autologous blood transfusion is not immunologically neutral but has intrinsic immunomodulatory potential. Therefore we investigated in vivo different immunological mediators in 56 randomized patients of a study comparing autologous and allogeneic blood transfusion in colorectal cancer surgery. Soluble IL-2 receptor, which is an indicator of general immune activation and the following immunologic refractory phase, indicated immunosuppression was more elevated at the seventh postoperative day in patients with allogeneic transfusions (p = .013) and autologous transfusions (p = .0003). The immunologic determination of TNF-alpha showed a significant postoperative increase in patients with autologous transfusions only (p = .0031). However, postoperative increase of soluble TNF-receptors p55 and p75 was also significant in patients transfused with allogenic blood (p = .022; p = .0014). The response to tetanus toxoid vaccination, an indicator of humoral immunity, was higher in patients transfused with allogeneic rather than autologous blood (p = .082), whereas responses of patients with autologous transfusions were even lower than in nontransfused patients. The reciprocal was already found for cell-mediated immunity determined by epicutaneously tested delayed-type hypersensitivity-reactions. IL-10 levels, an indicator of cellular immunosuppression, were determined in 27 additional patients before operation, immediately postoperative, and at the seventh postoperative day. IL-10 was found elevated immediately postoperative in allogeneic (p = .011) and nontransfused patients only (p = .042). The data from this study substantiate recent findings of a different immunomodulatory potential of allogeneic and autologous blood transfusion. They furthermore support the hypothesis that autologous blood transfusion does not contain immunologically neutral effects of allogeneic blood, but itself exerts an immunomodulatory effect.
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PMID:Modulation of immune response by blood transfusion: evidence for a differential effect of allogeneic and autologous blood in colorectal cancer surgery. 942 52

Virus-associated hemophagocytic syndrome (VAHS) is a disorder characterized by benign generalized histiocytic proliferation and marked hemophagocytosis associated with systemic viral infection. An immunodeficiency which includes an extremely decreased leukocyte and platelet count together with abnormalities in the CD4/CD8 ratio are the most common features of VAHS. Here we report an early-onset periodontitis (EOP) patient with VAHS from the standpoint of host-parasite interaction to understand the effect of this systemic disorder which might possibly influence susceptibility to periodontal disease. The patient is a 16-year-old Japanese male clinically diagnosed as having generalized EOP with slight gingival inflammation and moderate bone loss. This patient manifested VAHS at 3 years of age, and then had an unusual 4 recurrences (at 5, 7, 11, and 14 years old). Laboratory tests conducted include: 1) complete blood analyses: 2) peripheral neutrophil functions (chemotaxis, phagocytosis, superoxide production, and adherence); 3) peripheral lymphocyte subpopulations and functions, T-cell proliferative activity and productivity of cytokines (interleukin-2 [IL-2], interferon gamma [IFN-gamma], and tumor necrosis factor alpha [TNF-alpha]); 4) serum cytokine levels (IL-1 beta, IL-2, soluble IL-2 receptor [sIL-2R], IL-4, IL-6, IFN-gamma, and TNF-alpha; 5) serum immunoglobulin G (IgG) antibody titers against periodontopathic bacteria; 6) serological human leukocyte antigen (HLA) typing; and 7) determination of bacterial flora of the periodontal pockets. The results indicated that the patient's neutrophil chemotaxis and random migration were below the normal range. In lymphocyte examinations, T-cell proliferative activity, IL-2, and IFN-gamma productivity were elevated. Serum IFN-gamma level was also significantly higher than normal range. No specific periodontopathic bacteria were predominant in the periodontal pockets, however, the serum IgG titer against Porphyromonas gingivalis was elevated throughout the examination period. It is suggested that VAHS might be a possible risk factor for periodontal disease, and hence may serve as a model in understanding the role of host defense mechanisms in the establishment of inflammatory periodontal disease.
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PMID:Host defensive, immunological, and microbiological observations of an early-onset periodontitis patient with virus-associated hemophagocytic syndrome. 944 99


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