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)

In these experiments, we tested in various in vivo assays the immune responses of inbred C3H/HeN(MTV-) (C3H-) mice during carcinogenesis by chronic exposure to UV irradiation. Although the UV-treated mice were unable to reject syngeneic UV-induced tumor transplants, they rejected H-2-incompatible tumor allografts and H-2-compatible skin allografts. The primary hemagglutinin response to sheep red blood cells was normal in these mice, as were the induction of a local graft-versus-host reaction with lymphoid cells from UV-irradiated donors and the induction of an inflammatory response to dimethyl sulfoxide in the footpads of UV-treated mice. An early transient depression of two reactions in UV-irradiated mice occurred: delayed hypersensitivity to dinitrochlorobenzene measured by footpad swelling and the graft-versus-host reaction in UV-irradiated recipients measured by the use of the popliteal lymph node weight gain assay. Both of these reactions returned to a normal level before the development of primary tumors. We conclude that the inability of UV-irradiated mice to reject syngeneic and autochthonous UV-induced tumors was not due to a generalized immunosuppressive effect of chronic UV irradiation.
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PMID:In vivo immune responses of mice during carcinogenesis by ultraviolet irradiation. 2 May 14

The most important mechanisms for the specific depression of immune reactions--immuno-tolerance, enhancement, transfer of antibodies, drug induced tolerance, immunological suicide, application of antibody-toxin-complexes--are discussed with regard to their possible application in the clinical practice. A tentative hypothesis for induction of antigen specific suppression is proposed, basing on the use of antigen-immunosuppressive agent-conjugates (AIC). Antigen binding lymphocytes are supposed to bind the AIC and to pick them up through endocytosis. After breakdown of the AIC in the lymphoid cells the free immunosuppressive agent can become effective causing damage to the specific cell clones.
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PMID:[Modification of the immune reaction by antigen-immunosuppressive-agent conjugates. I. Tentative hypothesis for the induction of antigen-specific suppression by antigen-immunosuppressive-agent conjugates]. 6 72

The immunological responsiveness of a panel of 17 patients with systemic lupus erythematosus (SLE) was studied in an in vitro model of xenogeneic sensitization against mouse lymphoid cells. Generation of cytotoxic thymus-derived (T) cells evaluated by a chromium release assay against labeled target cells was found to be drastically impaired in these lupus patients. Such depression was independent of drug therapy at the time of the study, clinical status, and other immunological parameters such as antibodies against native DNA, complement levels, cryoglobulinemia, circulating immune complexes, or T- and bone marrow-derived (B)-cell numbers. In contrast to the cytotoxic response, the proliferative responses to phytohemagglutinin, to allogeneic lymphocytes, and to xenogeneic lymphocytes were not significantly different from those of normal individuals. The latter response was shown to be H-2 restricted with the primed lymphocyte test. These results suggest the presence of a selective defect in the generation or in the expression of killer cells rather than a deficiency in antigen recognition by T cells. The role of serum factor(s) was examined by educating the lymphocytes of normal subjects in the presence of serum from SLE patients. Such manipulation affected both the generation of killer cells and the proliferative response. Finally our observations indicate that depression of cell-mediated immunity in SLE patients may be associated with several mechanisms including a cellular one, specifically affecting the generation of killer T cells, and a humoral one possibly as a result of antilymphocytic antibodies and(or) immune complexes.
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PMID:Selective depression of the xenogeneic cell-mediated lympholysis in systemic lupus erythematosus. 11 Aug 33

The long term alterations of T and B lymphocytes in the peripheral blood of patients treated with regional irradiation for various malignancies were examined. Eighty patients were tested at various intervals after the completion of irradiation. Absolute lymphocyte counts, the percentages of T cells and B cells, and the blastogenic response to phocyte reaction (MLR) were determined. Nearly all patients initially had absolute lymphocytopenia and one-third of the patients tested 3 years after completion of irradiation had lymphocyte counts which were more than two standard deviations below the normal range. The depression was not specific for either the T-or B-lymphocyte subpopulations. The PHA response was impaired for extended periods of time after the completion or irradiation. Differences in the mean response of lymphocytes to PHA were noted for all concentrations of the mitogen, but were most marked with suboptimal concentrations of PHA. The MLR was below the lower limits of normal in 70% of the recently irradiated patients. There was a gradual recovery of the ability to respond in the MLR, and all patients tested more than 4.5 years after the completion of therapy had a normal response. These results were compared with those obtained in patients treated with total lymphoid irradiation for Hodgkin's disease. Although three appeared to be a difference in the effect of radiation on lymphocyte subpopulations in the two groups, the effects on lymphocyte function were similar.
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PMID:The long term effects of radiation of T and B lymphocytes in the peripheral blood after regional irradiation. 14 54

The effect of intravenous injection of 10(6) BALB/c spleen cells into C57B1/6J recipients was assayed by both mixed lymphocyte culture (MLC) of recipient lymphocytes, and by grafting donor (BALB/c) thyroids into recipient mice. It was observed that a single intravenous injection produced depression of proliferative and cytotoxic T cell responses in MLC of spleen, lymph node and peripheral blood lymphocytes of the recipients. This effect was specific for the sensitizing genotype (MLC of recipient and third-party CBA/H lymphocytes was unaffected), and persisted for several days after sensitization. The pattern of this diminished response suggested that the effect was due to a combination of recruitment of reactive lymphocytes from peripheral lymphoid populations, and the generation of alloantigen (H-2?)-specific suppressor T cells in the spleen. In contrast to these findings in vitro, a similar sensitization led only to accelerated rejection of thyroid allografts in vivo.
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PMID:Effect of in vivo exposure to allogeneic cells upon subsequent in vitro T cell responses and upon allograft rejection. 14 61

Changes in T-and B-lymphocytes content in experimental benzene intotication (BI) of CBA-mice were studied. The content of spontaneously rosette-forming cells, B-lymphocytes with C3 -receptors and T-cells in macro-and microtest was determined. It was shown that BI resulted in disorders in the function of thymus, depression of T-cell system and autoimmune shifts. A number of characteristics in kinetics of various fractions of lymphoid cells due perhaps, to different sensitivity of particular types of lymphoid cells to benzene and compensatory response as well. The significance of described phenomena is discussed.
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PMID:[Change in the content of T-and B-lymphocytes in experimental benzene poisoning (author's transl)]. 15 75

Following administration of deuterium to white rats changes of dysimmunitary-immunitary depression occurred. At the beginning the changes involved the whole spleen parenchyma, with marked lymphocyte depopulation of the red pulp and a decrease of the lymphod follicles. After about 4 - 7 days important amorphous deposits were formed, located exclusively perifollicularly and only in the spleen. The authors suggest the dysimmunitary globulinic-paraamyloidic nature of these deposits which, in their opinion, are produced by deuterium through a chemical mechanism. The differential diagnosis was only made with Gamma-Gandy nodules, because no such changes are found in pathology. It is not known why this deposition takes place exclusively in the spleen and especially around the lymphoid follicles. The authors raise the question whether some methods could be found which might direct the immunitary blockade to certain organs.
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PMID:Influence of deuterium on the spleen immune system. 16 Sep 93

Neither activation nor depression of murine peritoneal macrophages or lymphoid cells modified the suppressive effect of the virus-inhibiting factor or interferon on the multiplication of Ehrlich's ascitic cancer cells in mice.
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PMID:[Role of host cells in suppression of the in vivo multiplication of Ehrlich's ascitic cancer cells by the virus-inhibiting factor or interferon]. 16 Nov 94

The effects of two immunotherapy regimens on the development of an untreated, uniformly lethal transplantable line-10 hepatoma in strain 2 guinea pigs were monitored during treatment of an identical tumor 10 cm away. Line-10 cells were injected intradermally simultaneously at each of two sites. When one site was treated 6 and 16 days later with rabbit antibody against guinea pig fibrin fragment E, the complete regression of the treated tumor, a 25--30% depression in the development of the untreated tumor, and an increased survival time were observed. In another group of animals, when one site was treated 5 days after tumor challenge with syngeneic or xenogeneic "tumor-immune" RNA in a regimen including syngeneic nonsensitive lymphoid cells and tumor-specific antigen, all animals survived after complete and apparently specific regression of the tumors at both the treated and untreated sites. For the RNA regimen, we have shown that immunotherapy of an intradermally established line-10 tumor results in complete abrogation of both the treated and a distant untreated tumor; i.e., demonstrating a systemic effect.
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PMID:Tumor regression at an untreated site during immunotherapy of an identical distant tumor. 17 71

Although elevated antibody levels to the Epstein-Barr virus (EBV) have been reported in a number of lympho-proliferative neoplasms, it has not been possible to determine whether these antibodies were the result of a specific response to an oncogenic agent (EBV), whether they were a non-specific humoral compensation for depressed cell-mediated immunity (CMI), or whether a different mechanism was responsible. We have previously shown in a group of lymphoma patients that depressed cellular immunity to a number of standard antigens (Candida, SKSD, etc.) is not associated with an increase in antibody to EBV. In this study, we tried to compare CMI to possible EBV and lymphoid cell line antigens with humoral antibody to EBV. The two basis CMI assays utilized were lymphocyte cytotoxicity (LC) and skin testing (ST) for delayed hypersensitivity. In the LC assay, an EBV-containing cell line (F265) was used as the target. Reactivity against F265 was stronger in normal individuals than in cancer patients, suggesting a relationship to general cellular immune competence. ST studies showed that membrane extracts from lymphoid cell lines derived from patients with Burkitt's lymphoma and nasopharyngeal carcinoma (NPC) were more likely to elicit a delayed hypersensitivity in lymphoma and NPC patients than cell lines derived from normal individuals. Patients with ST reactivity against the membrane preparations from the tumour-derived cell lines were as likely to have elevated EBV antibodies as patients without such reactivity. The data strongly indicated that the elevated EBV titres in lymphoma patients are not related to a specific or non-specific depression of CMI.
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PMID:Humoral and cellular immunity to EBV and lymphoid cell line antigens in human lymphoma. 19 66


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