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)

With increasing time in culture and increasing mitotic number there is a decreased sensitivity of BALB/c mouse embryo fibroblasts (MEF) to the effects of the culture supernatant from concanavalin A stimulated splenocytes. When exposed to culture supernatant in vitro for 16 h 'old' MEF (12 days in culture at 37 degrees C with three subcultures) showed less increase in class I major histocompatibility complex antigens (H-2Kd and H-2Dd) than 'young' MEF (up to 8 days in culture at 37 degrees C with two subcultures). The subculture number alone was not the cause of decreased sensitivity to culture supernatant, since MEF subcultured five times over 5 days in vitro did not exhibit it. We propose that the insensitivity to the major histocompatibility complex increasing effects of culture supernatant precedes cell senescence and discuss how it could contribute to depression of cell-mediated immunity in aged animals.
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PMID:Age decreases the capacity of mouse embryo fibroblasts to increase surface H-2 when stimulated with concanavalin A-induced splenocyte culture supernatant. 393 72

During 15 years of inbreeding of pigs (Canadian Landrace) a semi-inbred line has been developed. The inbreeding coefficient (FX) is 0.84, which theoretically corresponds to between 8-9 generations of brother/sister matings. At the highest inbreeding level (0.84) the mean number of newborn piglets in the litter was 7.2 (5 litters, n = 36) including 5 stillborn (13.8%). The mean birth weight of the litter was 8.56 kg (5 litters, n = 31) the mean piglet birth weight was 1.23 kg and at the age of 21 days the mean weight of a litter was 33.24 kg with a mean piglet weight of 5.44 kg. During inbreeding, immunogenetic alloantigenic systems were investigated. Of 15 known erythrocyte systems, alleles of loci J, K, and of the most polymorphic system E, segregated. As to other immunogenetic systems (histocompatibility, leucocyte and allotypes) 2 SLA haplotypes (major histocompatibility complex) and 2 alleles of the SLC leucocyte system segregated. Allotransplants of the skin in SLA compatible siblings survived for a mean of 50.7 days (n = 77) compared with 10.8 days (n = 29) in non-inbred siblings. Tests of blastic transformation activated by T and B lymphocyte mitogens revealed a normal cell-mediated immune response. After immunization with some cell membrane alloantigens a normal humoral response was also recorded. All tested animals were halothane-resistant and tolerated a 10-min exposure to 5% without developing malignant hyperthermia. Depression due to inbreeding was manifested by a reduced reproductive ability (smaller number of piglets, frequent incidence of gonadal hypoplasia, diminution or loss of libido).
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PMID:Development of a semi-inbred line of Landrace pigs. I. Breeding performance and immunogenetic characteristics. 406 54

We have studied the occurrence of two phenotypic components (pancreatic lymphocytic infiltration [PLI] of the pancreas and T lymphocytopenia) of the spontaneous insulin-dependent diabetic syndrome (IDDM) in the progeny of hybrids obtained by crossing BB diabetic rats with rats of inbred strains differing from the BB rat at the major histocompatibility complex, RT1. Both PLI and T lymphopenia were seen in animals with all three possible genotypes in both (BUF x BB) and (LEW x BB) lines. PLI was seen in all IDDM animals. T lymphopenia was strongly associated with overt IDDM in both lines (chi 2 = 22.28, p = 0.00002 and chi 2 = 19.28, p less than 0.00001). In addition, T lymphopenia was associated with PLI with and without IDDM in both lines (chi 2 = 8.32, p = 0.0039 an chi 2 = 3.95, p = 0.0467). Not all animals exhibiting PLI without overt IDDM had depressed T cells. Not all animals with T lymphopenia had PLI with or without IDDM. In both lines, the overt IDDM occurred only in animals with at least one RT1 u haplotype derived from the BB rat, confirming our previously reported association of IDDM and RT1. We interpret this evidence to suggest that the overt IDDM syndrome requires one MHC-linked gene and at least two non-MHC-linked genes, which determine susceptibility to PLI and to circulating T lymphocyte depression.
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PMID:Spontaneous diabetes mellitus syndrome in the rat. II. T lymphopenia and its association with clinical disease and pancreatic lymphocytic infiltration. 633 14

Microglial cells account for approximately 20% of the total glial population in the central nervous system. They are distributed with no significant local differences in the white and grey matters. In contrast to astrocytes they cover non-overlapping territories. They belong to the mononuclear phagocyte system and form the resident macrophages in the brain tissue, the spinal cord and the retina. Their function in the normal neural parenchyma is unknown. However, in various pathologies they form a most reactive sensor to threats to the nervous system. Within a few hours they exhibit an activation program that we have studied in seven different experimental paradigms, e.g. following nerve section, direct brain trauma, toxic lesion, spreading depression, ischemic lesion, fiber degeneration, autoimmune diseases. Activated microglial cells become immuno-competent and are MHC (major histocompatibility complex) class 1 and class 2 positive. They express the amyloid precursor protein, APP. The complement receptor CR3bi is quickly upregulated. The mitotic activity depends on the colony stimulating factors M-CSF and GM-CSF and the appropriate receptors. Molecules discussed as signals in the activation process of microglia are cytokines such as IL-1, IL-2, IL-6, TGF beta 1. An important role could also be attributed to the unique potassium channel of microglia. Brain macrophages of microglial origin have a strong respiratory burst activity, meaning that they produce oxygen radicals. They also possess Cathepsin B and L and thus are potentially cytotoxic. Taken together, microglia are highly reactive, mobile and multifunctional immune cells of the CNS that can play a universal role in the defence of the neural parenchyma.
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PMID:Microglia, the first line of defence in brain pathologies. 776 26

Evidence from the house mouse (Mus) suggests that the extreme diversity of genes of the major histocompatibility complex (MHC) results from three different forms of selection involving infectious disease (pestilence), inbreeding (incest) and MHC-based mating (sexual) preferences. MHC-based disassortative mating preferences are presumed to have evolved because they reduce homozygosity throughout the genome, and particularly within loci linked to the MHC. Progeny derived from such disassortative matings would enjoy increased fitness because of both reduced levels of inbreeding depression and increased resistance to infectious disease arising from their increased MHC heterozygosity.
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PMID:Evolution of MHC genetic diversity: a tale of incest, pestilence and sexual preference. 812 7

In a previous investigation, we obtained evidence that the major histocompatibility complex (MHC)-restricted proliferative response of CD4+ lymphocytes to Mycobacterium paratuberculosis antigens was depressed in naturally infected and immunized animals. Findings suggested that depression of the response was attributable to an abrogation in the ability of CD4+ cells to respond to specific antigens and/or the actual loss of antigen-reactive cells. In vitro cell experiments indicated that the depression was associated with the presence of gamma/delta+ T cells that modulated CD4+ cell function. Examination of additional animals confirmed and extended these observations and showed that the ability of gamma/delta+ T cells to regulate CD4+ responses were blocked by the presence of CD8+ cells. CD4+ T cells from some exposed animals incorporated [3H]-thymidine in the presence of CD8+, gamma/delta+ cells and/or antigen and antigen-presenting cells, but CD4+ cell proliferation was abrogated when CD8+ were excluded from the assays. Likewise, gamma/delta+ T-cell proliferation was abrogated when CD8+ cells were present. The mechanism by which CD8+ cells blocked gamma/delta+ T-cell responses could not be determined, however, the observed effect resembled the veto cell phenomenon. The data suggest that the development of protective immunity against M. paratuberculosis may be dependent on the capacity of CD8+ cells to modulate the regulatory activity of gamma/delta+ T populations.
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PMID:The cellular immunology of bovine paratuberculosis: immunity may be regulated by CD4+ helper and CD8+ immunoregulatory T lymphocytes which down-regulate gamma/delta+ T-cell cytotoxicity. 836 13

Some widely used psychoactive drugs, such as tricyclic antidepressants and antipsychotic phenothiazines exhibit iatrogenic effects on the thyroid. These side effects may arise from interactions at different steps of thyroid hormone biosynthesis. These drugs can induce a change in iodine capture by thyroid cells or can complex iodine, making it unavailable for thyroid hormone synthesis and thus decreasing thyroid hormone blood levels; they can also inhibit thyroid peroxidase activity and thus T3 and T4 synthesis or enhance deiodination of T4 to T3 or to Rt3 by stimulation of deiodinase activity. Moreover, tricyclic antidepressants interfere with the hypothalamic-pituitary-thyroid axis via the noradrenergic or serotonergic systems and might therefore decrease T4 or T3 blood levels, respectively. Phenothiazines can induce autoimmune hypothyroidism, as shown by an increase in the expression of the major histocompatibility complex antigen and by a production of antithyroglobulin or antithyroperoxidase antibodies. However, all these mechanisms are only speculative in humans, as they have only been demonstrated in vitro or in animal experiments. Clinically, thyroid function and affective disorders are closely linked. On one hand, the therapeutic response to antidepressants could be influenced by the thyroid status; on the other hand, the larger the thyroxin decrease induced by antidepressants, the better the therapeutic effect might be. Moreover, cotreatment with thyroid hormones and antidepressant drugs could allow either a decrease in the rate of treatment failure or a faster recovery from depression. As antipsychotic or antidepressant treatments are administered over long periods in humans, their thyroid toxic effects must be taken seriously.
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PMID:Relationship between psychotropic drugs and thyroid function: a review. 957 80

Bovine viral diarrhea virus (BVDV) infection altered leukocyte populations in calves that were reflected by depression of T, BoCD4+, and BoCD8+ lymphocytes in the thymus and depression of B lymphocytes in Peyer's patches (PP). The present study was based on mononuclear leukocyte preparations from eighteen 9- to 12-month-old crossbred calves that were each exposed to either bovine respiratory syncytial virus (BRSV), BVDV, or BRSV and BVDV concurrently, or served as mock-infected controls. Peripheral blood leukocytes were collected on postinfection days (PID) 0, 2, 4, 6, and 8, and cell populations from thymus, spleen, mesenteric lymph node, and PP were collected at necropsy on PID 9. The leukocytes were analyzed using flow cytometry for lymphocyte subpopulations expressing antigens specific for BoCD2, BoCD4, BoCD8, BoWC1, lambda light chain of bovine immunoglobulin, BoCD11b and major histocompatibility complex (MHC) class II. Concurrent BRSV and BVDV infections caused exaggerated alterations in leukocyte populations with a greater percentage of T-lymphocytes harvested from the PP. Alterations in the leukocyte populations in lymphatic tissues and in peripheral circulation due to BVDV infection may be an important mechanism for causation of clinically severe diseases of the respiratory and digestive tracts during concurrent BRSV and BVDV infections.
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PMID:Alteration of leukocyte populations in calves concurrently infected with bovine respiratory syncytial virus and bovine viral diarrhea virus. 1063 Jul 91

Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).
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PMID:Functional requirement for class I MHC in CNS development and plasticity. 2443 53

Immune responses represent a source of systemic stress which impacts the brain and modifies various neuroendocrine and behavioral functions. Therefore, the immune system has been conceived of as a potential contributor to stress-related behavioral abnormalities, such as depression. Much of this knowledge has been gained through research focused largely on the administration of cytokines and/or bacterial endotoxin (eg., LPS), which targets innate immune cells, such as macrophages. However, fewer studies have addressed the effects of T cell activation on central nervous system (CNS) function. The discovery and characterization of bacterial superantigens (SAgs) has introduced an important opportunity for studying how T cell activation influences CNS function. Superantigens target unique variable regions of the beta chain of the mouse and human T cell receptor. This is restricted by the class II molecule of the major histocompatibility complex (MHC), and results in the production of a cytokine cascade that includes interleukin-2 (IL-2), interferon-gamma (IFNgamma), tumor necrosis factor (TNF) and many other cytokines, including IL-6. The best studied SAgs are the staphylococcal enterotoxins, of which staphylococcal enterotoxins A and B (SEA and SEB), have been shown to produce significant changes in behavior and activation of the hypothalamic-pituitary-adrenal (HPA) axis. Importantly, a T cell requirement was necessary to produce these changes. Furthermore, the anorexic or hypophagic effects of SAg challenge in mice appears to be related to anxiety-like processes, since challenge with both SEA or SEB reduces consumption of mainly novel food or food presented in a novel context. In the present paper, these studies are reviewed and related to known alterations in both anxiogenic and anxiolytic neuropeptides. It is suggested that immunologically-induced changes in the brain activate both categories of neuropeptides, thereby sustaining an adaptive state of arousal that promotes appropriate behavioral adjustments during infectious illness.
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PMID:Neural and behavioral responses to systemic immunologic stimuli: a consideration of bacterial T cell superantigens. 1577 53


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