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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following an intradermal immunization of guinea pigs with dinitrophenylated bovine gamma globulin (DNP23-BGG), human serum albumin (HSA) and trinitrophenylated sheep red blood cells (TNP-SRBC) emulsified in complete or in incomplete Freund's adjuvans the effectivity of 6-mercaptopurine (6-MP) on the formation of specific antibodies was investigated. By application of 10 mg 6-MP/kf/day--in guinea pigs a significant depression of antibody formation against BGG could be demonstrated if treatment is started on the day of antigen injection and continued for seven days. The production of anti-SRBC agglutinating antibodies was only suppressed if the antigen was injected together with complete Freund's adjuvans. The anti-DNP and anti-HSA antibody formation was not influenced by this kind of immunosuppressive treatment.
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PMID:[The influence of 6-mercaptopurine on the humoral immune response in guinea pig. 1. The importance of antigen and adjuvans (author's transl)]. 6 95

The immunodepressive effect of Toxoplasma gondii infection in mice was studied, using sheep erythrocytes (SRBC) as the testing antigen and serum hemagglutinins, hemolysins, and both direct and indirect splenic plaque-forming cells (PFC) to SRBC as assays. In the primary antibody response, immunoglobulin M (IgM), hemagglutinins, and hemolysins and both IgM- and IgG-secreting PFC were depressed in animals immunized after infection. Maximum immunodepression occurred during the first 3 weeks of Toxoplasma infection. When the secondary antibody response was studied, results varied. Mice immunized with SRBC after being infected with T. gondii had a depression in both IgM and IgG PFC. Mice immunized with SRBC before being infected with T. gondii and then given a challenge dose of SRBC had a delay, but no an actual depression, in IgG hemagglutinins and hemolysins and IgG-secreting PFC. These studies show that the immunodepression associated with Toxoplasma infection is complicated, and they provide no definitive explanation for the mechanism.
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PMID:Depressed antibody responses to a thymus-dependent antigen in toxoplasmosis. 31 57

The in vitro anti-SRBC response of several murine strains declined markedly with age in parallel with an increase in the activity of suppressor cells in the spleen and bone marrow which prevented early events during the induction of the immune response. These suppressor cells released soluble mediators and lacked the characteristics of mature T cells or macrophages. In addition the suppressor cell in the bone marrow could be removed on anti-Ig columns and fractions of old splenic suppressor cells sedimenting at 0.32 cm/h were greatly enriched in surface Ig bearing cells. Old immunodepressed mice did not lack potentially immunocompetent cells since the antibody response of old spleen cells could be restored by specifically activated T cells or lipopolysaccharide which act on B cells. These results suggest that a rise in the activity of non-T suppressor cells in the spleen and bone marrow may account, in part, for the depression in humoral immunity observed in aging mice.
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PMID:Immunological senescence. I. The role of suppressor cells. 36 7

Chronic pre- and postnatal exposure of CD rats to low levels of lead resulted in a marked depression in the antibody response to SRBC as well as decreased serum IgG levels. Serum IgM and IgA levels were normal. The fact that the antibody response to LPS, a thymus independent antigen, was not altered, suggested that the T-lymphocyte rather than the B-lymphocyte is affected by lead exposure. Additional significance is lent to these results when blood lead levels in treated rats were found to be similar to levels found in many children in urban areas.
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PMID:Depression of humoral immunity in rats following chronic developmental lead exposure. 36 64

Mice exposed to a compound containing three phenol derivatives by being housed in cages washed with dilute solutions of the compound, developed considerable depression of the ability to generate plaque forming cells (PFC) in response to sheep erythrocytes (SRBC) in vitro after a four week exposure. The depression became more severe with continued exposure up to fourteen weeks. Administration of orthophenylphenol (OPP), the most abundant derivative in the mixture, resulted in a similar immunodepression at 10 ppm and a slight depression at 1 ppm. Numbers of FcR+ lymphocytes and of macrophages did not appear to be affected by this treatment. The response to a T-dependent and a T-independent antigen were affected similarly, although the latter was depressed less markedly than the former. While these data are only preliminary, they suggest that studies should be performed in detail to elucidate the immunodepressive effects of compounds which are in wide use as household and institutional disinfectants.
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PMID:Phenol derivatives are immunodepressive in mice. 54 52

The effect of Lewis lung tumor growth in mice on the induction of primary immune response to SRBC, was investigated by PFC assay for measuring antibody activity and by footpad test as a correlate for delayed type hypersensitivity reactions. With the appearance of micrometastases in the lungs there was a decline in the humoral and cellular immune response to the SRBC. An increase of number and size of metastases in the lungs led to a further depression of the immune reactivity. Since the reduction of general immune response in mice bearing this tumor is not due to a direct influence of tumor cells, it might be assumed that suppressor cells or factors, are actively abrogating the general and also the tumor directed immune reactions.
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PMID:Correlation of immune response with clinical stage in Lewis lung tumor-bearing mice. 70 36

Malaria-induced immunosuppression has been demonstrated in humans and experimental animals. The suppressed immune response has been suggested to be primarily humoral and not cellular in nature, since classical lymphocytic cell-mediated responses have been reported to be normal. Since previous results have demonstrated that an impairment in macrophage antigen processing may be a contributing factor in malaria-induced immunosuppression, the present studies were conducted to determine if the macrophage/reticuloendothelial system (RES) alteration occurs parallel to the course of the malarial infection and if the impairment in antibody formation is temporally related to the RES alteration. The present study has demonstrated that a profound impairment in splenic direct plaque forming cell (PFC) formation occurs in malaria-infected Balb/c mice which had been immunized with sheep erythrocytes (SRBC) either 2 or 4 days after inoculation with Plasmodium berghei, NYU-2 strain. Serum hemagglutinin titers were significantly depressed in mice which received the SRBC 4 days post-inoculation; however, no alterations in antibody titers were observed in mice immunized with SRBC 2 days post-inoculation. Coincident with the depression of serum antibody titers at the day 4 immunization period was a profound increase in the vascular clearance of 51Cr-SRBC with an enhanced hepatic uptake of the 51Cr-SRBC and a decreased splenic localization of the labelled erythrocytes. It is suggested that a direct vascular exposure of the splenic lymphoid-macrophage elements to the parasite may be responsible for the initial early alterations in the PFC response while the impairment in serum antibody titers and splenic phagocytic activity may be a result of the pathological alterations occurring later in the infection, e.g., tissue anoxia, anemia, and hemolysis.
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PMID:A temporal relationship between reticuloendothelial system phagocytic alterations and antibody responses in mice infected with Plasmodium berghei (NYU-2 strain). 76 77

Using a microculture system which permits the survival of very small numbers of active lymphoid cells, the frequency of units of response towards two non-crossing antigens, SRBC and phage phi17, is determined in long term cultures of calf lymph node cells. A much higher frequency, as hitherto reported using mouse spleen cells, is found: about one active unit of response towards either antigen per 8 x 10(3) cells. When microcultures are stimulated with the two antigens, phenomena of antigenic competition occur: a 40% depression of the response to each antigen takes place when the antigens are added simultaneously or when the second antigen is added at a later time within the first 2 days. When the interval between the two stimulations is 3 days, only the response to the first antigen takes place at the same level of frequency as that obtained from cultures which are stimulated only with this antigen. These results support the hypothesis of pluripotentiality of lymphoid cells. Each immunocompetent cell would contain a large repertoire of specificities; triggering with antigen would provoke a two stage differentiation process. The first stage lasting until 48 hours after stimulation would be reversible, whereas the second stage would be irreversible. The latter step would involve the phenomena of specific antibody synthesis. Theoretical implications of these results are discussed.
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PMID:The repertoire of specificity of lymphoid cells: primary response and antigenic competition in microcultures. 78 43

Pseudomonas aeruginosa infection depresses contact sensitivity to 2-phenyl-4-ethoximethylene-oxazolone (oxazolone), and enhances the antibody response to sheep erythrocytes (SRBC) in the mouse. Anti-oxazolone antibody titres were found not to be significantly different in infected and uninfected animals; thus, the major circulating classes of antibodies do not seem to be responsibile for the observed depression of skin reactivity. Low dose (20 mg/Kg) cyclophosphamide (CY) pretreatment induced a further potentiation of antibody response to SRBC, and prevented depression of contact sensitivity in infected mice. On the other hand, when infected animals were pretreated with high doses (200 mg/Kg) of CY, antibody production was completely suppressed, whereas contact sensitivity was unaffected. Since CY treatment is known to selectively inhibit B lymphocytes, and since it can abrogate the infection-induced depression of reactivity to oxazolone, it is suggested that suppressor cells, which may have B-cell characteristics, are stimulated during P. aeruginosa infection in the mouse.
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PMID:Evidence for suppressor cell activity associated with depression of contact sensitivity in Pseudomonas aeruginosa infected mice. 99 63

The number and distribution patterns of lymphocytes in the spleens and lymph nodes of Balb/c mice which express immunoglobulin surface receptors were studied in terms of the effects of a murine leukemia virus on the immune-response mechanism. Friend leukemia virus induces a prompt, marked depression of the immune response of mice to antigens such as sheep erythrocytes and E. coli LPS. A functioning T- and B-lymphocyte system is necessary for the response to the SRBC's whereas E. coli LPS, a T cell-independent antigen, stimulates B cells alone. Although the responses to both classes of antigen were markedly depressed in FLV-infected mice, the major defect appeared to be impairment of B-cell function, at least early in the course of infection. In order to examine in more detail the mechanism of interaction between FLV and lymphoid cells with Ig surface receptors, presumably B cells, immmunofluorescent analyses were performed with spleen, and lymph node cells from FLV-infected mice. Within a few days after infection there was a marked decrease in the percentage of spleen cells with Ig surface molecules, although the absolute number of these cells was either unchanged or increased due to marked splenomegaly caused by the virus. A marked decrease in the percentage of splenocytes with theta antigen, considered a marker for mature T cells, also was evident in infected mice. The number of spleen cells showing evidence of FLV infection (i.e., positive for FLV-associated antigens) increased rapidly during the first few days after infection, and within 2 to 2 1/2 weeks nearly all of the nucleated splenocytes were positive for the tumor antigen. In contrast to the results for spleen cells, there were increases rather than decreases in the percentages of Ig-positive and theta-positive cells in the lymph nodes after infection. The number of lymph-node cells that showed the presence of FLV antigen was much lower than in the spleen, and their appearance was also much slower as the leukemic process progressed. Despite these differences between spleen and lymph-node cells in terms of relative percentages of Ig- and theta-positive lymphocytes, relatively similar depressions were evident for the percentages of lymphoid cells that could redistribute their surface Ig receptors into polar caps when incubated with anti-Ig serum at 37 C. Marked impairment of the Ig-capping responses for both spleen and lymph-node cells paralleled the course of infection and development of immunosuppression. These observations indicate that murine leukemia virus infection can both alter the responsiveness of immunocompetent cells to T-dependent and independent antigens and depress the number and normal functional activity of these cells, as reflected by altered surface Ig receptors and antigens.
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PMID:Lymphocyte surface receptors and leukemia virus-induced immunosuppression. 109 86


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