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 elucidate the mechanisms underlying trauma-induced immunosuppression and decreased IL-2 production we evaluated: 1) the effect of trauma on IL-1 production at different time intervals and 2) the effect of IL-1 in vivo administration on immune functions (IL-1 production, IL2 production, NK cell cytotoxicity) in normal and traumatized mice. Experiments were performed on CBA/H mice a) subjected to scald injury (sacrificed 3 h and 6 h later) b) treated with IL-1 in vivo (human recombinant IL-1 beta 100 ng/mouse, sacrificed 21 h and 24 h later) and c) subjected to both IL-1 in vivo treatment and scald (IL-1 was given 18 h before scald, animals were sacrificed 3 h and 6 h after scald i.e. 21 h and 24 h after IL-1 administration). Our results demonstrate that trauma alone increases IL-1 production from 1 h to 24 h after trauma infliction. Recombinant IL-1 given in vivo also induces a significant rise in IL-1 production. When mice were subjected to both trauma and IL-1 in vivo treatment, the rise in IL-1 production was not additive. Trauma induced severe depression of IL-2 production which could not be overcome by in vitro addition of IL-1 to IL-2 producing splenocytes from traumatized mice. In contrast, IL-1 administered in vivo stimulated IL-2 production in normal mice, and when given prior to trauma infliction, it completely abrogated trauma-induced suppression of IL-2 production. The same effect was seen on NK cell cytotoxicity (an IL-2 dependent function).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-1 in vivo modulates trauma-induced immunosuppression. 212 99

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

Lymphokine-activated killer cells generated from peripheral blood of Non-Hodgkin's lymphoma patients showed comparable levels of cytotoxicity. The patients with advanced disseminated disease displayed better augmentation with recombinant interleukin-2 (rIL-2) than the patients with localized disease. Thus, the defective cytotoxic potential of patients could be corrected in a culture of effector cells with IL-2. The indigenous ability to produce IL-2 in response to activation of peripheral blood mononuclear cells with phytohemagglutin showed slight depression and a positive correlation with the stage of the disease. Phenotypic analysis revealed a heterogenous population of cells involved in cytotoxic activity. Thus, IL-2 merits further evaluation in malignant lymphomas, particularly in relation to other variable therapies in conjunction with chemotherapy.
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PMID:Generation and characterization of lymphokine-activated killer cells from non-Hodgkin's lymphoma patients. 238 64

Immunosuppressive mechanisms loom as important factors in depression of delayed-type hypersensitivity responses during active tuberculosis. Nonspecific suppression may be mediated by circulating immune complexes containing mycobacterial polysaccharides such as D-arabino-D-galactan. The mechanism of suppression involves activation of monocyte production of immunosuppressive prostaglandin E2. Peripheral blood mononuclear cells from patients with tuberculosis include increased numbers of monocytes that suppress the response to tuberculin purified protein derivative (PPD). Antigen-specific suppression is associated with monocyte activation by a number of criteria, including decreased surface expression of HLA-DR determinants and increased production of interleukin 1 (IL-1). The increased production of IL-1 is associated with--and may have a causal relation to--immunosuppression. A second parallel regulatory mechanism involves PPD-specific suppression by Fc gamma receptor-bearing lymphocytes. The consequence of these immunosuppressive circuits is depression of tuberculin-induced blastogenesis, production of IL-2, and generation of IL-2 receptors. These findings suggest that natural infection with Mycobacterium tuberculosis may result in immunosuppression. Studies of potentially protective antigens in experimental systems must be designed to assess and avoid activation of suppressor circuits.
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PMID:Immunologic aspects of mycobacterial infections. 246 22

After peroral infection with cysts of Toxoplasma gondii, C57BL/6 mice died and A/J mice survived. To better understand the reasons for this difference in survival, host defenses during acute infection were studied: initial portal of entry of T. gondii contributed to susceptibility as more C57BL/6 mice survived after i.p. than peroral infection (p less than 0.001). Susceptible (C57BL/6) mice had more necrosis and inflammation in their brains, livers, and mesenteric lymph nodes than resistant (A/J) mice. Susceptible mice had less IgM antibody to T. gondii (p less than 0.0005) than resistant mice 7 days after infection, but amounts of IgG antibody to T. gondii were similar. Infection reduced percentages of spleen cells with the Lyt-2+ phenotype in susceptible (p less than 0.02) but not resistant mice; infection decreased percentages of spleen cells with the L3T4+ phenotype similarly in both strains of mice. Spleen cells from infected susceptible mice had greater depression in their blastogenic response to Con A (p less than 0.05) and produced significantly more IFN-gamma in culture with (p = 0.009) or without (p less than 0.05) Toxoplasma Ag than spleen cells from infected resistant mice. Infection increased serum levels of IFN-gamma substantially in susceptible but not resistant mice. Lymphocyte IL-2 production was similar in both groups of mice. Peritoneal macrophages from both strains of mice became activated to inhibit or kill T. gondii by 7 days after infection, but Kupffer cells became activated only in susceptible mice. These results indicate that increased resistance to peroral Toxoplasma infection is likely to be mediated by a number of immune responses acting together. They suggest that increased susceptibility may result from inadequately regulated inflammatory responses that increase tissue destruction.
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PMID:Immune responses associated with early survival after peroral infection with Toxoplasma gondii. 249 63

Chemical sympathectomy of adult mice with 6-hydroxydopamine (6-OHDA) either prior to or following epicutaneous sensitization with the trinitrophenyl (TNP) hapten decreased the delayed hypersensitivity (DH) response to ear challenge. To determine if uptake of 6-OHDA into sympathetic nerve terminals, and their subsequent destruction, was required for suppression of DH, the catecholamine uptake blocker, desipramine, was employed to block 6-OHDA-induced sympathetic denervation. Pretreatment with desipramine prevented the depression of DH. In vivo treatment with the beta blocker, propranolol, did not alter the 6-OHDA effect, eliminating the potential contribution of released catecholamines, acting on beta-adrenoceptors, to DH reduction. Sympathectomy before sensitization also diminished hapten-specific T cell reactivity of sensitized lymph node (LN) cells, as measured in vitro by IL-2 production and CTL generation. In vivo DNA synthesis in draining LN in response to immunization was modestly decreased following 6-OHDA. Thus, sympathetic denervation appears to impair T cell activity in vivo and in vitro. Overall, these results indicate the SNS plays a role in generation of cell-mediated immunity.
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PMID:Sympathetic neural modulation of the immune system. I. Depression of T cell immunity in vivo and vitro following chemical sympathectomy. 250 10

Measurements were made of cellular immune system parameters in a group of healthy medical students. On the basis of psychosocial stress encountered during a five-day topic-centered self-awareness course, we investigated modulation in immunity in relation to personality characteristics. 6 days before the beginning of the seminar personality profiles were drawn and blood samples taken. Further immunological measurements were made on day four of the seminar and three weeks after its conclusion. On the fourth day of the seminar we observed throughout the group higher lymphocyte and suppressor/cytotoxic T lymphocyte counts in comparison with counts one week earlier, and likewise a heightened responsiveness to PHA- and IL-2 stimulation. The T lymphocyte counts had dropped. In subjects with a higher need for succorance/nurturance, the depression of the immune system was manifested in a drop in the helper/inducer T lymphocyte counts, and in the more achievement- and order-oriented subjects in a downregulation as observed by higher suppressor/cytotoxic T lymphocyte counts. Our results show that under psychosocial stress, healthy people experience on the one hand an activation of the immune system, and on the other hand an immunodepression bearing a specific relation to personality characteristics.
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PMID:[Selective effect of personality markers and psychosocial stress on T lymphocyte subpopulations]. 252 32

The effects of delta-9-tetrahydrocannabinol (THC) on NK cell activity were studied. Previously, we reported that incubation of human peripheral blood mononuclear cells in THC resulted in an inhibition of natural killer (NK) cell activity. The present study examined the mechanism(s) of the decrease in NK cell activity. The inhibition of killing by NK cells was not due to a failure of NK cells to bind to K562 target cells. Furthermore, indomethacin did not abrogate the THC-mediated effect, suggesting that prostaglandins are not involved in the process leading to suppression of NK cell activity. However, NK activity was partially restored if cells, pretreated with THC, were washed to remove excess drug and then incubated overnight in fresh medium before assay. Addition of 1-100 U IL-2, either during pretreatment with THC or during overnight incubation, precluded or promoted the reversal of the inhibition of NK cell cytotoxicity. We conclude that the regulatory mechanism(s) involved in depression of NK cell cytotoxicity by THC is significantly influenced by IL-2.
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PMID:Prevention and reversal of delta-9-tetrahydrocannabinol induced depression of natural killer cell activity by interleukin-2. 254 Jan

The recent progress in immunology has shown depression of immunological competence, especially cellular immunity in tumor bearing host due to anesthesia, blood transfusion and operative trauma itself and disappearance of host's concomitant immunity caused by removal of primary tumor, resulting the enhancement of growth of residual tumor or metastatic foci. The prophylactic lymph node dissection in cancer operation must be reconsidered through immunological studies of lymph node as immunological surveillance system. Splenectomy combined with the operation of stomach cancer must also be reconsidered. Therefore, the main aims of this society are to suppress the negative aspect in connection with the cancer operation by means of immunotherapeutic approach and to prevent the recurrence and/or metastasis of cancer. Research society, met for the first time in 1980, and has since discussed the following main themes at 9 occasions of meetings up to 1988: 1. Pre- and postoperative immunological competence in cancer patients. 2. Surgery and immunological competence for cancers. 3. Antitumor activity of regional lymph nodes. 4. Splenectomy and tumor growth. 5. Surgical treatment and immunochemotherapy. 6. Serum immunosuppressive factors in cancer patients. 7. BRM and immunotherapy. 8. Diagnosis and treatment of cancer using monoclonal antibody. 9. Cancer treatment using IL-2, TNF. 10. Host defense factors and cancer metastasis. In addition, 14 educational lectures dealing with recent immunology have been given by immunological specialists.
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PMID:[On the activity of the Japanese Research Society for Surgical Cancer Immunology]. 273 30

(LEW X BN)F1 cardiac allografts are rejected within 8 days in untreated LEW recipients. At the critical time point of 5 days after transplantation, the obviously rejecting grafts are enlarged and maximally infiltrated by host cells as shown by 111In-labeled lymphocyte tracer studies. However, when such hearts were retransplanted back to naive (LEW X BN)F1 secondary hosts, they survive indefinitely, showing that even late rejection is reversible in the absence of sustained host immunological drive. Attempts were then made to abrogate this advanced immune responsiveness using Cyclosporine (CsA). CsA therapy (15 mg/kg/day for 7 days) starting from day 5 produced indefinite graft survival, similar as if initiated at the time of operation. Addition of exogenous IL-2, which drives the proliferation of Tc, could not reverse this effect. Serial changes in phenotype of lymphocyte subpopulations infiltrating both acutely rejecting and indefinitely functioning cardiac allografts in unmodified and CsA treated hosts, respectively, were then studied. Ratio of Th:Tc/s cells in acutely rejecting grafts was 1.6 by day 3; it inverted abruptly to 0.7 by day 5-6, suggesting predominance of Tc/s during the later stages of allograft rejection. Similarly, treatment with CsA produced a transient depression of Th, with recovery of original Th:Tc/s ratio during the next 2-3 weeks. Adoptive transfer experiments were then performed to investigate the functional significance of these findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:T suppressor lymphocytes reverse ongoing acute allograft rejection. 293 14


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