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)

To assess the immune system status, the authors have measured various lymphocyte populations, whose ratio was determined in indirect immunofluorescence with Ortho or BL monoclonal antibodies, CD3, CD4, CD8, and DR-specific. The detected shifts in the immunity system permitted dividing the patients into 3 groups: Group 1 consisting of subjects with moderate immunity depression, Group 2 including those with moderate immunity stimulation, and Group 3 comprising patients with poorly manifest changes in the immunity system. The authors recommend carrying out analyses of the immunity system before and after implantation surgery, for such analyses may help predict possible complications and improve therapeutic correction thereof.
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PMID:[Changes in the immune system of patients with dental implants made of different materials]. 225 4

We describe 40 HIV-seropositive patients who developed visceral leishmaniasis. All the patients lived in areas endemic for visceral leishmaniasis and belonged to groups at risk for AIDS. Twenty-three patients (57.2%) had definitive AIDS before or after diagnosis of leishmaniasis and 77.5% were classified as belonging to CDC group IV. Fever was present in 95% patients and enlargement of the liver and/or spleen in 92.5%. Lymphopenia was found in 78.3%, depression of the absolute number of CD4 lymphocytes in 90% and depression of the CD4 to CD8 ratio in all evaluated cases but leishmania antibodies were found in only 35.2%. Parasites were demonstrated in the bone marrow or liver in every case. Thirty patients (75%) showed an initial good response to antimonial drugs, although the leishmaniasis followed a chronic or relapsing course in 17 (42.5%). HIV-related mortality was 40%. A significant correlation was found only between the relapsing course of the disease and mortality. In a multivariate linear regression model, the relapsing course was the only variable that influenced mortality. Visceral leishmaniasis is an opportunistic disease that should be suspected in HIV-infected patients. We suggest that it should be included in the CDC group IV C-1 and considered as a disease indicative of AIDS.
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PMID:Visceral leishmaniasis in patients infected with human immunodeficiency virus. Co-operative Group for the Study of Leishmaniasis in AIDS. 227 73

One of the major limitations in the use of triazene compounds for inducing increased immunogenicity of tumor cells in vivo (i.e. chemical xenogenization) is the profound immunodepressive activity of these drugs. The present study analysed the inhibitory effects of DTIC on various T-dependent immune responses in mice in an attempt to determine the mechanism of action and appropriate treatments for reverting the immune damage produced by the agent. Results obtained show that treatment with DTIC in vivo produced: (a) inhibition of spleen cell proliferation; (b) reduced IL-2 production in response to allogeneic stimuli; (c) reduction of the generation of IL-2R + CD8 + cells in allogeneic MLC; (d) inhibition of allo-CTL generation. The addition of IL-2 to MLC on day 2 of the co-culture restored full allogeneic CTL responses. These data suggest that exogenous IL-2 could be used to counteract DTIC-induced depression of T-cell reactivity, which is presumably involved in hosts' responses against autochthonous xenogenized tumor cells.
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PMID:IL-2 reverses the inhibition of cytotoxic T-cell responses induced by 5-(3,3' dimethyl-1-triazeno)-imidazole-4-carboxamide (DTIC) in vitro. 229 62

The activation of T lymphocytes by an antigenic challenge requires that the CD3 T cell receptor alpha/beta (TcR) is bound to an appropriate ligand, i.e. major histocompatibility complex antigen, on an antigen-presenting cell. In addition, numerous studies suggest that the accessory molecules CD4 and CD8 participate in the recognition process, and may have inhibitory as well as augmenting effects depending on the ways in which they participate. In the present study we attempt to define the conditions by which CD8 exerts enhancing and inhibitory effects on resting CD8+ T cell activation, and which parameters of activation are regulated through participation of CD8/CD4. We find that experimental procedures leading to TcR-CD8 aggregation induce T cell activation whereas experimental procedures preventing TcR-CD8 aggregation inhibit T cell activation. CD8/CD4-induced variations in the extent of T cell activation are apparent as variations in interleukin 2 (IL 2)-dependent growth and in the number of blastoid cells bearing IL 2 receptors. Inhibition of CD8+ T cell activation is successful only if the majority, if not all CD8 molecules are occupied by soluble antibody. This latter finding argues against the suggestion of other groups that CD8 may be a receptor for negative signaling. Rather, the results support the alternative notion that a basal level of TcR-CD8 aggregation, existing in the resting state or induced by TcR-ligand interaction, is an essential prerequisite for CD8+ T cell activation. Enhancement or depression of this basal level of aggregation causes facilitation or inhibition, respectively, of activation. This may be a mechanism for the regulation of IL 2-dependent clonal expansion of T cells in immune responses.
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PMID:Immunoregulation through CD8 (Ly-2): state of aggregation with the alpha/beta/CD3 T cell receptor controls interleukin 2-dependent T cell growth. 249 22

Sixty-five patients with recrudescent orofacial herpes simplex virus (HSV) infections all had circulating HSV-specific antibody measured by ELISA and cell-mediated immunity (CMI) to HSV by in vitro lymphoproliferation. Thirteen control subjects with no history of HSV were negative for both tests. Thirty-three patients, repeatedly investigated during 6 to 38 months, had between 1 and 8 recrudescences each. Lymphoproliferative responses to HSV were low during recrudescence, rose to a peak a few weeks later and then declined to a positive background level. However, ELISA titres and lymphoproliferative responses to concanavalin A were high throughout, and peripheral blood mononuclear cell (PBMC) subset numbers measured by fluorescent flow cytometry remained within normal limits. During HSV lesions, depressed lymphoproliferation to HSV was abrogated by removal of CD8+ T cells from PBMC either by using a panning technique (nine patients) or by cell sorting (three patients). Reconstitution of the CD8-depleted population suppressed the lymphoproliferative response to HSV. Depletion of CD8+ T cells did not affect lymphoproliferation to HSV outwith recrudescence (four patients), nor lymphoproliferative responses to another antigen (PPD; five patients) during recrudescence. Thus, reduced lymphoproliferation to HSV during recrudescence may be due to HSV-specific CD8+ suppressor T lymphocyte function, rather than lack of HSV-responsive lymphocytes. This may result in depression of normal CMI responses to the virus during an asymptomatic recurrence allowing recrudescent lesions to develop.
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PMID:Variation in lymphoproliferative responses during recrudescent orofacial herpes simplex virus infections. 255 8

In an area endemic for visceral leishmaniasis, 16 patients with human immunodeficiency virus (HIV) infection developed the disease. All belonged to populations at risk for AIDS (15 were intravenous drug abusers). Five patients fulfilled the criteria for full-blown AIDS, and two more fulfilled them after diagnosis of leishmaniasis. All presented with the classic manifestations of visceral leishmaniasis, but leishmania serology was negative in 15 patients (93%). Leishmania donovani amastigotes were identified in the bone marrow in all cases. Most patients responded initially to treatment with pentavalent antimonial drugs, but seven (43%) followed a chronic course, with multiple relapses in five, despite alternative treatments. Visceral leishmaniasis occurred in patients with different levels of depression of the CD4 to CD8 lymphocyte ratio. Mortality was 37% (six patients) and was independent of the chronic-relapsing course of the disease. In no case was leishmaniasis the primary cause of death. Our data establish that visceral leishmaniasis is an opportunistic infection in HIV-infected patients, and we suggest that in endemic areas it should be considered an indicator disease for the diagnosis of AIDS.
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PMID:Visceral leishmaniasis (kala-azar) as an opportunistic infection in patients infected with the human immunodeficiency virus in Spain. 210 72

A brief characterization of 27 neurologic syndromes occurring in 44 AIDS patients during two years is presented. In 4 out of 7, intrathecal Ig synthesis was demonstrated without the CSF cell count and blood brain barrier values being within a normal range. Ig intrathecal formation was also observed in 2 LAS patients without neurological symptoms. Similar changes in CSF findings occur in other subacute encephalitis, particularly in multiple sclerosis. Activation of CSF B-cells or their depression due to impairment of CD8 T-lymphocytes was indicated as the cause of this phenomenon. In the Authors' opinion this explanation is somewhat general. The possibility of an immune response in CNS was clearly demonstrated, but in the CSF neither B-cells nor Ig producing plasma cells are evident. In addition, it should be noted that the reliability of blood brain barrier and Ig intrathecal assessment procedures is doubtful in ADC disease, because of the severe alterations in serum albumin and Ig concentrations seen in these patients.
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PMID:Cerebral spinal fluid IgG production in HIV-positive patients. 274 Jun 4

Levels of T lymphocytes were measured in 20 consecutive patients, 18 men and two women, supported with ventricular assist devices or an artificial heart. Indications for support were bridge to transplantation (n = 10), postcardiotomy cardiogenic shock (n = 8), and acute myocardial infarction shock (n = 2). Control levels were from healthy volunteers not undergoing cardiac operation. Preoperatively, numbers of total lymphocytes and subclasses CD3, CD4, and CD8, as well as the interleukin-2 receptors (IL2R), were the same as controls (cells/microliters): lymphocytes, 1,940; CD3, 1,413 +/- 410; CD4, 894 +/- 318; CD8, 490 +/- 185; IL2R, 96. From implant to postoperative day 5, levels were below control values (p less than 0.001), reaching a nadir on postoperative day 2 (lymphocytes, 896 +/- 599; CD3, 489 +/- 267; CD4, 309 +/- 207; CD8, 183 +/- 107; IL2R, 43 +/- 47). Data from 10 patients (group 1) who survived (four weaned from cardiopulmonary bypass, six transplanted) were compared with those from 10 patients (group 2) who died of multiorgan failure, sepsis, or both. From preimplant through postoperative day 6, levels did not differ between groups. However, from postoperative day 7 to the last day of ventricular support (group 1, 24-90 days; group 2, 7-29 days), group 1 levels (lymphocytes, 2,364 +/- 618; CD3, 1,825 +/- 553; CD4, 1,013 +/- 187; CD8, 796 +/- 402) were significantly above (p less than 0.01) group 2 levels (lymphocytes, 1,290 +/- 463; CD3, 746 +/- 295; CD4, 534 +/- 253; CD8, 221 +/- 106). These data indicate that lymphocytes and particularly T cells 1) decrease after ventricular assist device insertion, reaching a nadir at postoperative day 2, 2) return to control values after patients whose clinical status improves, and 3) remain low in severely ill patients. T-cell depression in ventricular assist device patients is related to the severity of the patient's condition rather than the presence of the device.
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PMID:T cells in ventricular assist device patients. 280 99

The kinetics of the cellular and humoral responses of 30 recipients of hepatitis B vaccine were studied. All individuals exerted an HBsAg blastogenic response sometime throughout the study period but the maximum response was detected on day 28 and 56. The removal of CD8+ cells enhanced significantly the HBsAg response at the times tested, whereas treatment with anti-CD4, anti-CD8, C' and anti-CD4+ C' had no effect. Vaccination also led to the depression of phytohaemagglutinin (PHA) blastogenic response. This response was maximally suppressed 4 to 8 days after immunization at least for the primary and secondary responses and 28 days after the third dose of vaccine. The humoral response to HBsAg was detected only after the second dose of vaccine was given. The results suggest that a CD8+ cell controls the magnitude and intensity of the HBsAg blastogenic response, which may help to explain why several investigators had not been able to detect this response in hyperimmunized individuals. Primary immunization with HBsAg does lead to an expansion of B memory since a secondary response anti-HBsAg was observed.
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PMID:Humoral and cellular immune responses by normal individuals to hepatitis B surface antigen vaccination. 296

Spontaneous improvement of active juvenile rheumatoid arthritis (JRA) occurred after T lymphocytosis in an 8-year-old boy. He had prominent lymphocytosis, the count reaching 59,000/mm3, followed by spontaneous disappearance of fever, arthralgia, lymphadenopathy, hepatomegaly, and C-reactive protein. The serum immunoglobulin levels were gradually decreased. The surface marker analysis, using two color flow cytometry, showed that the lymphocytes were activated suppressor T lymphocytes, expressing CD3, CD8, HLA-DR, and CD8 plus CD11. When studied in vitro with pokeweed mitogen stimulation, the T lymphocytes significantly suppressed the immunoglobulin production by autologous B lymphocytes as compared with the T lymphocytes at remission (p less than 0.01). Based on the widely believed notion that depression of suppressor T lymphocyte functions is one of the important mechanisms underlying systemic JRA, the activated T lymphocytosis with the suppressor phenotype and suppressive function on the immunoglobulin production may have been related to the improvement of active JRA in the patient.
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PMID:Spontaneous improvement of juvenile rheumatoid arthritis after T lymphocytosis with suppressor phenotype and function. 297 87


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