Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 54-year-old asymptomatic male patient was followed for more than 7 y and presented a constant T cell lymphocytosis without skin involvement or bone marrow depression. No clinical or haematological aggravation was noted during this follow-up. Morphologically, the cells were large granular lymphocytes strongly positive for beta-D-glucuronidase, negative for acid phosphatase and with features of T cells on transmission and scanning electron microscopy. The immunological studies of the lymphocytes showed the following parameters: E rosettes+, mouse rosettes-, SmIg-, OKT3+, OKT4+, OKT8-, OKT6-, Ia-, TdT-, NK-, HTLV-, decreased PHA and PWM stimulation, no interleukin 2 production and failure to enhance Ig synthesis in a PWM driven system. The karyotype was normal. This case of chronic T cell lymphocytosis with large granular lymphocytes helper profile and defect of helper function, not reported in the literature, may correspond to a distinct entity in the heterogeneous group of chronic T cell disorders.
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PMID:Chronic T cell lymphocytosis with large granular lymphocytes of helper (OKT4) phenotype. 298 13

The mechanism by which prostaglandin E2 (PGE2) inhibits human T lymphocyte activation and proliferation was studied. We analyzed the effect of physiologic concentrations of PGE2 on interleukin 2 (IL 2) production, expression of IL 2 receptor (Tac antigen), and expression of the transferrin receptor after in vitro activation with phytohemagglutinin. PGE2 inhibited T lymphocyte proliferation by 80 to 90% of control values. This was associated with a similar degree of inhibition of IL 2 production while the expression of IL 2 receptor was not affected. This was in marked contrast to the expression of the transferrin receptor, which was inhibited 65% after 72 hr of in vitro activation. The addition of exogenous, purified IL 2 reconstituted lymphocyte proliferation to 50% of control values, but had no effect on transferrin receptor expression. Because PGE2 is known to increase the intracellular concentration of 3',5' cyclic adenosine monophosphate (cAMP), we investigated the effect of another adenylate cyclase activator, i.e., isoproterenol, as well as the effect of extracellular administration of the cAMP derivative dibutyryl cAMP (dBcAMP) on IL 2 production, Tac antigen expression, and transferrin receptor expression. It was demonstrated that isoproterenol, as well as dBcAMP, inhibited transferrin receptor expression on PHA-activated T lymphocytes to the same extent as PGE2, and exogenous IL 2 could not counteract the down-regulation of the receptor expression. In contrast, neither isoproterenol nor dBcAMP had any significant effect on IL 2 receptor expression. Prostaglandin F2 alpha (PGF2 alpha), which has been reported to elevate intracellular cyclic GMP levels, had no effect on lymphocyte activation and proliferation, and did not counteract the PGE2-induced depression in IL 2 production. In contrast to its effect on peripheral blood lymphocytes, PGE2 had no effect on transferrin receptor expression or cell proliferation by IL 2-dependent T cell clones and IL 2-independent T cell lines. These studies demonstrate that PGE2 exerts its inhibitory effects on T cell activation and proliferation via two distinct pathways: inhibition of IL 2 production and inhibition of transferrin receptor expression. The transferrin receptor inhibition is mediated via the cAMP pathway and is IL 2-independent.
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PMID:Prostaglandin E2 acts at two distinct pathways of T lymphocyte activation: inhibition of interleukin 2 production and down-regulation of transferrin receptor expression. 298 62

Phytohemagglutinin (PHA)-induced interleukin 2 (IL-2) production and lymphocyte proliferation were measured in former workers of the Okunojima Poison Gas Factory (poison gas workers), who have a high incidence of lung cancer, and the efficacy of administration of Nocardia rubra cell wall skeleton (N-CWS) was studied. In comparison with normal controls and poison gas workers receiving N-CWS, lymphocyte proliferation in poison gas workers not receiving N-CWS showed a significant decrease, while IL-2 production showed a slight though not statistically significant decrease. When N-CWS was administered to poison gas workers, IL-2 production and lymphocyte proliferation were significantly elevated, with a peak two weeks after administration. N-CWS, by elevating IL-2 production of lymphocytes, is considered to have improved the depression of lymphocyte proliferation.
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PMID:Effects of Nocardia rubra cell wall skeleton on interleukin 2 production and lymphocyte proliferation in former poison gas factory workers. 308 31

We report four cases of Omenn's syndrome (OS), an autosomal recessive disease characterized by early erythrodermia, protracted diarrhea, severe infections, lymphadenopathy, hepatosplenomegaly, failure to thrive, and leukocytosis with marked eosinophilia. The immunological investigations revealed B lymphopenia with increased levels of serum IgE and marked depression of T-cell activation, not restored by the addition of exogenous interleukin 2 (IL-2). IL-2 and interferon-gamma (IFN-gamma) production in vitro were very low or absent. One patient was treated with HLA-identical bone marrow transplant with a complete remission of the clinical picture and the immunological defect. The infant died of graft versus host disease 4 months after the graft. For the remaining three infants the outcome was also fatal within the first year of life. In conclusion, OS should be considered a severe combined immunodeficiency disease with peculiar clinical, immunological, and histological findings.
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PMID:Clinical and immunological findings in four infants with Omenn's syndrome: a form of severe combined immunodeficiency with phenotypically normal T cells, elevated IgE, and eosinophilia. 311 64

Infection of mice with Trypanosoma cruzi results in a severe immunosuppression, accompanied by the appearance of autoimmune symptoms. We have previously shown that proliferation and interleukin 2 production by concanavalin A-stimulated T cells from infected mice is severely depressed. In this study we show that at least two phenomena are responsible for this depression. First, mixing experiments showed the existence, in spleens of infected animals, of adherent, Thy-1-negative and radioresistant suppressor cells. Second, studies of enriched T cell populations and analysis of precursors by limiting dilution showed that the T cell compartment itself was impaired in infected animals: responses of enriched T cells, even when reconstituted with normal accessory cells, reached only 40% of those obtained with normal uninfected mice.
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PMID:T lymphocyte function during experimental Chagas' disease: production of and response to interleukin 2. 315 31

Beta-2-adrenergic agonists are often employed in the treatment of acute bronchostenosis. Following our recent investigations into the influence of some drugs (cromolyn, ketotifen, theophylline) on the immune response, in this study we analyzed the in vitro effects of fenoterol (beta-2-adrenergic agonist) on the immune response. The mitogen-(PHA)-induced proliferation of peripheral mononuclear cells (PMNC), the PMNC proliferation induced by anti-T3 and anti-T11 monoclonal antibodies (MAbs), the PHA-induced lymphokine--interleukin 2 (IL-2) and interferon-gamma (IFN-gamma)--production were studied in ten healthy volunteers. Since the plasmatic peak of fenoterol following a single inhalation of 200 micrograms is about 20 ng/ml, in the experiments herein reported the drug was tested in the cultures at concentrations lower, equal and higher than the plasmatic peak: respectively, 2, 20 and 200 ng/ml. Furthermore, for a more detailed study of T-lymphocyte activities, we also evaluated the effect of fenoterol on T-cell clone proliferation. Our results, which reveal no effects of fenoterol on the studied immunological parameters, acquire relevance when related to our previous reports showing a depression of the immunological response exerted by theophylline and ketotifen.
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PMID:Fenoterol effects on the in vitro immune response. 317 57

The production of procoagulant activity by circulating monocytes and its regulation by a cytokine secreted by mitogen-stimulated peripheral blood mononuclear cells was investigated in recipients of HLA-identical sibling bone marrow transplants. Blood monocyte numbers reached the normal range within 3 weeks of transplant. After stimulation with lipopolysaccharide, macrophage procoagulant activity was found to be within the normal range in all patients at all times post transplant. It did not appear to correlate with the presence or absence of graft-versus-host disease. Surprisingly, and in marked contrast to our previously documented severe depression of interleukin 2 production by transplant recipients' peripheral blood mononuclear cells, the mitogen-induced production of the cytokine that induces procoagulant activity production (macrophage procoagulant inducing factor, MPIF) was also normal in the majority of patients when assayed using the responsive myelomonocytic cell line RC-2A. These findings suggest firstly that monocyte differentiation and function normalize rapidly post transplant; and secondly, when taken together with previous studies, that the ability of peripheral blood mononuclear cells to synthesize cytokines post transplant varies greatly according to the specific cytokine involved.
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PMID:Cytokine activity after human bone marrow transplantation. II. Production of macrophage procoagulant activity and the cytokine regulating its production, macrophage procoagulant inducing factor. 329 28

Depression of lymphocyte proliferative response occurs after trauma and hemorrhage. Because abnormalities in production or utilization of interleukin 2 (IL-2) can result in depression of mitogen-induced lymphocyte proliferation, we investigated the effects of unanesthetized hemorrhage on the generation of IL-2 by rat peripheral blood lymphocytes and the response of these cells to exogenous IL-2. Two hours after loss of 30% of total blood volume, IL-2 production was reduced by greater than 90%. Return to normal levels of IL-2 generation occurred by 48 hr after hemorrhage. Addition of purified rat IL-2 to cultures of phytohemagglutin-stimulated peripheral blood lymphocytes obtained from normal animals resulted in suppression of the proliferative response. Exogenous IL-2 produced a similar degree of suppression in the proliferation of cells obtained from hemorrhaged animals. These results show a profound hemorrhage-induced suppression of IL-2 generation, but no benefits of exogenous IL-2 in improving the depressed lymphocyte proliferative response that exists after hemorrhage.
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PMID:The role of interleukin 2 in hemorrhage-induced abnormalities of lymphocyte proliferation. 348 52

Depression of cell-mediated immunity in patients following severe traumatic injury has been well documented in vitro and in vivo. However, the exact mechanism of this defect is still controversial. In this study, we have investigated the ability of injured patients' peripheral blood mononuclear cells (PBMC) to produce two important immunoregulatory molecules, interleukin 1 (IL 1) and interleukin 2 (IL 2). Eighteen traumatic injury patients were studied during the course of their hospital stay and their results compared with a group of 18 normal age- and sex-matched controls. The results showed the following. (1) Production of IL 2 by normal PBMC in response to optimal doses of mitogen may vary with sex as well as age. (2) Adherent mononuclear cells from trauma patients produced at least as much IL 1 as normals. (3) IL 2 production, however, was markedly suppressed (normals, 1.6 +/- 0.2 U; traumatic injury, 0.6 +/- 0.1 U; P = 0.001) and persisted for as long as 50 days postinjury. OKT4+ cells were not significantly decreased at any time, nor were OKT8+ suppressor/cytotoxic cells increased at any time. Decreased IL 2 production in patients treated with steroids or those who were septic was not different from that in those patients who were not treated with steroids or were not septic. These results suggest that the cause of the defect in IL 2 production in traumatic injury patients is not related to a lack of the IL 1 signal, producer T cells, or Ia+ monocytes or to increased suppressor T cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of immunosuppression associated with severe nonthermal traumatic injuries in man: production of interleukin 1 and 2. 348 2

The influence in vivo of immunosuppressive drugs (cyclosporine, azathioprine, and corticosteroids) on the production of various lymphokines (alpha and gamma interferon, interleukin 2), both in organ transplant recipients and in normal volunteers taking 100 mg hydrocortisone orally has been studied. To avoid interference with the rejection process or viral infection, patients were studied in a steady state with low maintenance immunosuppression consisting of prednisolone combined with azathioprine or with cyclosporine. In patients treated with both drug regimens, significant depression of production of the three lymphokines was found. Normal volunteers challenged with 100 mg hydrocortisone showed inhibition of production of interleukin 2 and alpha and gamma interferon in 4 hr, a time corresponding to the nadir of T cell lymphopenia, affecting the OKT4 subset preferentially. The percentage of OKT8 cells remained unchanged. Percentages of large granular lymphocytes increased, but their absolute number was not significantly modified. Changes in lymphocyte markers were fully reversible after 24 hr, but interleukin 2 production remained markedly depressed, showing that the redistribution patterns induced by corticosteroids on lymphocyte subsets may be dissociated from functional consequences.
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PMID:Influence of in vivo immunosuppressive drugs on production of lymphokines. 391 67


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