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)

Standard immunological parameters measuring non-specific cellular immune reactivity were determined in 175 patients with different stages of gastric cancer prior to surgery and during follow-up. Several tests measuring monocyte activity were also employed. The total number of T cells and their subpopulations Ta and T29o was unchanged except depression of T29o in stage IV. The blastogenic response of lymphocytes to PHA as assessed by stimulation of protein synthesis was only depressed in stage IV. In contrast the PHA-induced lymphokine production was increased in all patients but the differences were significant for stage III and IV. Monocyte Fc receptor expression was increased in stages II-IV, while nitro blue tetrazolium reduction and antibody dependent cellular cytotoxicity of monocytes was elevated in stage IV. The number of extractable monocytes was not increased. Longitudinal studies suggested that most of the parameters normalized during follow-up. No major long-term impact of chemoimmunotherapy (5-FU + BCG) on the immune parameters was observed except a transient increase in PPD reactivity approximately 1 year after commencement of treatment. In patients with stage III gastric cancer the increased occurrence of suppressor cells (mostly monocytes) and elevated cytostatic activity of monocytes was associated with a longer survival while the increased lymphokine production and Fc receptor expression were seen in the group of patients succumbing earlier. We concluded that most of the changes in immune parameters were seen only in advanced disease and paradoxically disappeared in the course of disease. The determination of monocyte activity seems to be a sensitive indicator of immune system dearrangements in earlier stages of cancer and a useful prognostic factor in gastric cancer.
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PMID:Serial immunological testing in patients with gastric cancer. 348 1

Depression of the cellular immune responses in mice with disseminated histoplasmosis is associated with deficient production of interleukin-2 (IL-2) by splenocytes. Therefore, we examined whether a highly purified preparation of IL-2, recombinant human IL-2 (rIL-2), could modify the cellular immune responses in infected mice and whether this lymphokine could alter the severity of histoplasmosis in animals. Exogenous rIL-2, at concentrations of up to 1,000 U/ml, failed to augment the proliferative responses to concanavalin A by unfractionated splenocytes or splenic T cells from mice infected for 1 week. In addition, rIL-2 did not modulate the plaque-forming cell response to sheep erythrocytes by splenocytes from these same mice. However, at week 3, rIL-2 in concentrations ranging from 10 to 1,000 U/ml considerably augmented the proliferative response to concanavalin A and plaque-forming cell response to sheep erythrocytes by splenocytes from infected mice. Kinetics studies demonstrated that rIL-2 exerted maximal immunoregulatory activity when added on day 0 or 1 to cultures of splenocytes. In vivo administration of rIL-2, 200 to 20,000 U/day, for 10 days to normal and 3-week-infected mice did not alter the proliferative activity of splenocytes to concanavalin A; 200,000 U of rIL-2 per day actually depressed the proliferative responses of splenocytes from normal and infected mice. In vivo, rIL-2 did not modify delayed-type hypersensitivity responses to sheep erythrocytes or to histoplasmin by normal and infected mice. Moreover, treatment with rIL-2 in vivo did not reduce the number of Histoplasma CFU in spleens of mice. Thus, despite the immunoenhancing effect of rIL-2 in vitro, this lymphokine failed to exert similar effects in vivo.
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PMID:Modulation of cellular immune responses in mice with disseminated histoplasmosis by recombinant interleukin-2. 348 7

Pregnancy is a natural allograft and the mechanisms for its non-rejection are obscure. Depression of maternal cellular immunity was suggested as a possible explanation. Interleukin-2(IL-2) is a lymphokine release from OKT4+ lymphocyte. This factor has a crucial role in the proliferation and differentiation of T cell subsets, and controls functions associated with immune rejection mechanisms. We therefore examined the ability of lymphocytes from women in the 3 trimesters of pregnancy to produce IL-2 in culture. Mononuclear cells were cultured with PHA for 48 h. The IL-2-containing supernatant was added to and supported the proliferation of an IL-2 dependent T cell line. Proliferation of this line indicated the IL-2 content of the added supernatant. Using this assay, IL-2 production in all 3 trimesters of pregnancy was adequate and comparable to that of lymphocytes from non-pregnant women. These results suggest that the proposed defect in cellular immunity during pregnancy is not mediated by an inability of the lymphocytes to produce IL-2.
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PMID:Immunocompetence in pregnancy: production of interleukin-2 by peripheral blood lymphocytes. 350 Jul 80

The effects of cyclic nucleotides on the proliferation of cultured T-lymphocytes (CTC) stimulated by either phytohemagglutinin (PHA) or lectin-free interleukin-2 (IL-2) were studied. The addition of either N6,O2-dibutyryl cyclic AMP (DB-cAMP), aminophylline or isoproterenol to CTC cultures significantly suppressed the proliferation of CTC stimulated by either PHA or IL-2. This inhibitory effect was maximal when added at initiation of the assay; however, significant depression was still observed when added 24 h later. When DB-cAMP and aminophylline were added together, the inhibitory effects were additive. When DB-cGMP was added to the CTC cultures, inhibition of both PHA- and IL-2-stimulated cultures was also found, but the degree of activity was considerably less than for DB-cAMP or aminophylline. In contrast, when carbachol was added, no inhibition or modulation in proliferation was seen. Lastly, DB-cGMP was not found to antagonize the inhibitory effect of DB-cAMP, but instead to further increase the level of inhibition. In summary, these studies illustrate that cyclic nucleotides modulate the proliferation of IL-2-stimulated CTC as well as PHA-treated cells. This model system should provide an approach to study, in more depth, the mechanism by which cyclic nucleotides or their inducers can modulate the latter stages of the lymphocyte proliferative response, which is mediated by the lymphokine, IL-2.
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PMID:The effects of cyclic nucleotides on the proliferation of cultured human T-lymphocytes. 609 9

Human monocytes release a stable cytostatic factor during in vitro culture after stimulation with lymphokine and endotoxin. The cell cycle time of synchronized NHIK 3025 cells increased from 20.3 to 23.2 h in the first cell cycle when the target cells were exposed to the factor during the whole cell cycle. In exponentially growing NHIK 3025 cell cultures the cell doubling time increased from 18.9 h to 23.1 h under continuous factor exposure for 70 h. These cells regained normal cell division rate when fresh culture medium replaced the cytostatic factor. Continuous exposure to the cytostatic factor for 96 h increased the cell doubling time of asynchronous K-562 cells from 19.7 to 31.8 h. The target cell DNA synthesis, evaluated by thymidine incorporation, was markedly depressed after culture with the factor for 24 h, and this depression was detectable already within 4 h of culture. The factor showed no cytolytic effect on the two cell lines tested. The cytostatic factor influenced the cell cycle distribution of both target cells tested, since cell cycle analysis by DNA flow cytometry demonstrated a reversible inhibition of factor-exposed NHIK 3025 cells in G1- and early S-phase, whereas K-562 cells accumulated in G1-phase.
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PMID:Soluble cytostatic factor(s) released from human monocytes. II. Effects on target cell kinetics. 687 11

The fungal metabolite Cyclosporin-A (CyA) was investigated for its activity on several cell-mediated immune responses. Oral administration of 70 mg kg-1 of CyA for 5 days to C3H/HeN mice completely abolished the in vivo antigen-dependent production of a lymphokine capable of increasing macrophage cytotoxicity against tumor cells. Moreover, spleen cells from CyA treated mice were significantly depressed in their ability to produce in vitro lymphokines in response to PHA, whereas only a slight depression was observed when ConA was employed to induce lymphokine production. In parallel to the depression of proliferation-independent immune response, spleen cells from CyA treated mice showed a strongly depressed proliferative response to PHA, marginal reduction being observed in the response to ConA. B-lymphocytes did not seem to be affected by in vivo treatment with CyA, judging from the proliferative responses to LPS. Macrophage responses also remained unaltered after CyA treatment. No depressions in natural or lymphokine-induced macrophage cytotoxicity and in monokine production were in fact observed in CyA treated mice. Finally, a short-lived depression of natural killer (NK) activity was observed after CyA administration. These results indicate that in vivo CyA treatment selectively depressed cell-mediated functions of lymphocytes of the T-cell lineage. The hypothesis that T-cell lineage. The hypothesis that T-helper lymphocytes are the preferential target of CyA immunodepression is discussed.
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PMID:Effects of in vivo treatments with cyclosporin-A on mouse cell-mediated immune responses. 697 3

Cell-mediated immunity was studied by in vitro tests in seven patients with progressive multifocal leukoencephalopathy (PML). Lymphocyte proliferation in response to mitogenic stimulation was reduced to a variable degree in all patients, indicating a general impairment of cell-mediated immune responsiveness, although mitogen-induced production of the lymphokine migration inhibitory factor (LIF) was normal in most cases. Cell-mediated immunity to JC virus (JCV) was assessed by LIF production in response to JCV antigen. In the six PML patients tested, LIF production with JCV antigen was absent despite the presence of antibody to JCV in serum. This contrasted with positive LIF production in seropositive normal individuals and patients and patients with other diseases. These results provide the first in vitro evidence of a depressed cell-mediated immune response to JCV in patients with PML, and support the hypothesis that PML is accompanied by a selective marked deficiency in cellular response to this virus in association with a general depression of cell-mediated immunity of variable severity.
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PMID:Progressive multifocal leukoencephalopathy (PML): in vitro cell-mediated immune responses to mitogens and JC virus. 698 49

There was no difference in monocyte-mediated cytotoxicity between monocytes from patients with multiple myeloma or malignant lymphomas and monocytes from control persons after in vitro culture for 5 d. Cytostatic and cytolytic ability of lymphokine-activated monocytes cultured in medium with patient serum was significantly depressed compared to the ability of monocytes cultured with normal serum. A similar depression of cytostasis was found with non-activated monocytes of both patient and control origin. Sera from myeloma and lymphoma patients impaired the monocyte-mediated cytotoxicity equally.
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PMID:Inhibitory effect on monocyte-mediated cytotoxicity of sera from patients with multiple myeloma and malignant lymphoma. 715 89

A number of studies have suggested that the inflammatory and chemotactic autocoid platelet activating factor (PAF), together with various cytokines, plays an important role in the pathophysiology of trauma, sepsis, and shock. However, little is known about PAF's contribution to the immunosuppression associated with hemorrhage. The aim of our study was, therefore, to determine if the use of a PAF-antagonist following hemorrhage has any salutary effects on splenocyte lymphokine production. To study this, mice were bled to and maintained at a mean arterial pressure of 35 mm Hg for 60 min. The mice were then segregated into three groups and were resuscitated with shed blood plus lactated Ringer's solution (2x the volume of shed blood), containing either a potent PAF-antagonist (Ro 24-4736, a thienodiazepine) in dimethyl sulfoxide (DMSO) or DMSO-vehicle. Sham-operated mice received either DMSO-vehicle in saline or saline alone. Twenty-four hours thereafter the animals were sacrificed and splenocyte cultures established and stimulated for 48 hr with Con A (2.5 micrograms/ml). Supernatant lymphokine levels were determined by bioassay. The cellular release of interleukin-2 and -3 (IL-2 and IL-3) by splenocytes was significantly depressed in the nontreated or vehicle-treated hemorrhaged animals compared to shams. Treatment with the PAF-antagonist Ro 24-4736 restored IL-2 and IL-3 release values to levels comparable to those of the sham-operated animals. Thus, (1) PAF appears to play a significant role in hemorrhage-induced immunosuppression and (2) the use of a PAF-antagonist to uncouple the PAF-generated feedback loops prevents the depression in splenocyte function following hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:PAF-antagonist administration after hemorrhage-resuscitation prevents splenocyte immunodepression. 764 95

Cytotoxicity mediated by natural killer (NK) and lymphokine-activated killer (LAK) cells may be of significance in host defense against viral infections. This study included 347 patients infected with human immunodeficiency syndrome virus (HIV) type 1 and 110 controls. The NK cell activity, either unstimulated or stimulated with interferon-alpha (IFN-alpha) or interleukin-2 (IL-2), and the LAK cell activity were suppressed in patients, but the NK/LAK cell activity did not differ between patients with AIDS and patients without AIDS. However, the IFN-alpha-stimulated NK cell activity and LAK cell activity were reduced in patients with symptoms of HIV disease (CDCIV) when compared with asymptomatic patients (CDCII+III). When the data were analyzed by multiple linear regression, the percentage of CD4+ cells had a positive effect on these two parameters in patients without AIDS, whereas the percentage of CD4+ cells had no significant effect on unstimulated and IL-2-stimulated NK cell activity in these patients. In controls and AIDS patients, the percentage of CD4+ cells had no effect on NK/LAK cell activity in multiple linear models. The total number of CD16+ cells was low in patients compared to controls, whereas the percentages of CD16+, CD56+, and CD16+CD56+ were either normal or elevated. Therefore, the decrease in NK cell subpopulations did not contribute to the observed depression in NK/LAK cell activity in vitro. It is concluded that natural immunity is suppressed in HIV-seropositive patients primarily because of a qualitative defect of the NK/LAK cells. This qualitative defect includes a reduced responsiveness to IFN-alpha, which is progressive until the onset of symptoms, and possibly related to the loss of CD4+ cells.
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PMID:Defective natural immunity: an early manifestation of human immunodeficiency virus infection. 765 Apr 85


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