Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific pathogen-free B6D2 mice were infected intravenously with 10(8) viable BCG, M. habana or M. simiae and the level of tuberculin hypersensitivity to 2.5 micrograms PPD or cytoplasmic protein antigens (CPA) prepared from the other organisms was determined using the footpad swelling test with increasing time after infection. This was correlated with the growth or persistence of mycobacterial populations within the liver. Spleen cells were removed from these infected mice and the level of blast transformation following exposure to PHA, PPD or M. habana or M. simiae CPA was measured in vitro. Early in the mycobacterial infections (day 14) thymidine incorporation by the spleen cells was significantly enchanced followed by a profound depression in incorporation rates as the infection progressed. The mechanism of this depressed response involved the production of suppressor T cells in the spleen. In the case of the M. simiae or M. habana infection, cells capable of mediating suppression were still present even after 12 months of infection. In the BCG infection, suppressor T cells declined with time so that by 4 months incorporation rates were back to normal and suppressor cells were no longer detectable in the spleens of the infected animals.
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PMID:Development of suppressor T cells in mice heavily infected with mycobacteria. 644 70

Normal mice infected intravenously with 10(6) or 10(8) viable M. avium develop persistent infections of the lungs, liver and spleen. The liver and spleen counts remained relatively constant whereas those for the lung slowly increased until eventually some of the animals began to die as a result of the infection. None of the heavily infected mice developed delayed hypersensitivity (DTH) to the M. avium cytoplasmic protein antigen (CPA). Spleen cells harvested at increasing time periods after the M. avium infection were tested for their blastogenic responsiveness to PHA and M. avium CPA. The presence of suppressor T cells within the heavily infected spleens was demonstrated by means of cell-mixing experiments before and after treatment of the anergic spleen cells with anti-Thy-1.2 antiserum and complement. The specificity of the suppressor T cells was measured in terms of their ability to depress responsiveness to sheep erythrocytes and an allograft challenge. Initially, the suppressor T cell population affected all of the T cell-mediated responses but as the infection progressed, so the non-specific host responses tended to return gradually towards normal, whereas the specific M. avium CPA-mediated suppression persisted largely unchanged.
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PMID:The specificity of suppressor T cells induced by chronic Mycobacterium avium infection in mice. 645 15

Specific pathogen-free B6D2 mice were infected with 10(6) or 10(8) viable Mycobacterium bovis (BCG Pasteur) or Mycobacterium simiae and the in vivo growth curves were correlated with the levels of delayed hypersensitivity developed against a cytoplasmic protein antigen (CPA) injected into a hind footpad at increasing time intervals after infection. Half of the heavily infected, anergic mice were placed on a regimen of 10 mg of rifampin, 5 mg of amikacin and 2 mg of clofazimine per 100 ml of drinking water 2 or 8 weeks into the infection. The number of viable mycobacteria recovered from the lungs and spleens of the treated mice (compared with the corresponding drug-free controls) were reduced by up to 10,000-fold over a 3-month treatment period. Spleen cells were harvested at increasing time intervals from the drug-treated and control mice and T-cell enriched suspensions were tested for blastogenic responsiveness to phytohaemagglutinin (PHA) and to the specific CPA mitogen. The early (day 14) peak in tritiated thymidine ([3H]-TdR) uptake was followed by a sharp drop to near background levels. Cell-mixing experiments demonstrated the presence of a suppressor T-cell population in the heavily infected spleens of the M. simiae-infected mice. The suppressor-cell effect was substantially reduced following combined drug therapy although the specific CPA-mediated response was less affected than the non-specific PHA-mediated response.
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PMID:The effect of combined chemotherapy on suppressor T-cell activity in Mycobacterium simiae-infected mice. 645 54

Various species of atypical mycobacteria exhibited a wide range of growth patterns in the lung, liver, and spleen of specific pathogen-free B6D2 mice infected with these organisms. The growth varied from rapid elimination (complete avirulence) to a continued persistence in the lung, which eventually resulted in the death of many of the mice. Prior depletion of the T cells of aerogenically challenged mice did not affect the growth characteristics of the organisms within the lungs. Mice infected with Mycobacterium habana developed an early hypersensitivity response to the cytoplasmic protein antigens (CPA) of this organism, and this response was followed by a persistent state of anergy. Mice infected with Mycobacterium simiae failed to develop detectable levels of hypersensitivity at any time during the study. Spleen cells taken from mice infected with M. habana or M. simiae exhibited an early peak in the incorporation of [3H] thymidine after exposure of the cells to the nonspecific T-cell mitogen phytohemagglutinin (PHA). A similar peak occurred when the cells were exposed to the specific mitogen CPA of M. habana. Later in the infection, the anergic spleen cells showed no transformation of lymphocytes after exposure to either PHA or CPA. T-cell-mixing experiments, which were carried out both before and after treatment of suspensions of cells from the anergic spleens with anti-Thy 1.2 antiserum plus complement, indicated the presence of a population of suppressor T cells in the anergic animals.
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PMID:Immune responses to atypical mycobacterial lung infections. 646 12

A novel member of the Formin/Diaphanous family of proteins was cloned and characterized. A 4kB mRNA is ubiquitously expressed but is found in abundance in the spleen. FHOS (Formin Homologue Overexpressed in Spleen) contains a 3414bp open reading frame and encodes for an approximately 128kDa protein. FHOS has sequence homology to Diaphanous and Formin proteins within the Formin Homology (FH)1 and FH2 domains. FHOS also contains a coiled-coil, a collagen-like domain, two nuclear localization signals, and several potential PKC and PKA phosphorylation sites. FHOS-specific antiserum was generated and used to determine that FHOS is a predominantly cytoplasmic protein and is expressed in a variety of human cell lines. FHOS was mapped to chromosome 16q22 between framework markers WI-5594 and WI-9392.
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PMID:Identification and characterization of a protein containing formin homology (FH1/FH2) domains. 1035 28