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)

Further studies were carried out to investigate cellular sites of the resistance to the induction of immunological tolerance to HGG in DDD mice, assuming the presence of a subset of tolerogen-resistant splenic T cells. Spleen-seeking T cells were shown to be relatively resistant in comparison with lymph node-seeking T cells. The existence of a tolerogen-resistant T-cell subpopulation was indicated from the experiments demonstrating that tolerance was easily attained after adult thymectomy and that lymph node T cells became much more resistant to tolerance induction after adult splenectomy. The latter experimental result might also exclude the possibility of differences in microenvironment (probably in A cells) between spleen and lymph node. An attempt was made to investigate a possible involvement of A cells in the induction of tolerance. A cells were deprived in vivo by irradiation of the host 3 days prior to spleen cell transfer and in vitro by passing a spleen cell suspension through a Sephadox G-10 column. The deprivation of A cells resulted in priming of the host by the tolerogen rather than easier tolerance induction. No suppressive activity was observed in lymph node cells from tolerized mice. These results suggest that there exists a set of T cells, generated relatively recently in the thymus, preferentially migrating into spleen and there becoming resistant to tolerance induction.
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PMID:Studies on the resistance to tolerance induction against human IgG in DDD mice. II. Tolerogen-resistant T-cell population in the spleen. 8 82

Strain differences in the antibody response to human IgG (HGG) were observed when aggregated HGG was injected intravenously. Lipopolysaccharide (LPS) administered subsequently markedly enhanced the antibody response to HGG in low responder C57BL/6 mice as compared with that in high responder DDD, C3H/He or (C57BL/6 X DDD)F1 mice. Aggregate-free preparation of HGG at a dose of 0.5 mg induced immunological tolerance in all strains of mice tested. LPS injected subsequently converted tolerogenic, aggregate-free HGG into immunogen in DDD mice but not in C57BL/6 mice. To determine the correlation between adjuvanticity and mitogenicity of LPS, spleen cells from normal mice were cultured in the presence of LPS and 3H-thymidine uptake was measured. Spleen cells of DDD mice incorporated three times as much 3H-thymidine as those of C57BL/6 mice. There seems no strong correlation between both activities of LPS. The data obtained are discussed in terms of strain differences in the macrophage function for processing the antigen.
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PMID:Strain differences in the immunogenicity of aggregated human IgG and the adjuvant action of lipopolysaccharide on the low-responder strain of mice. 78 51

The effects of PCBs (polychlorinated biphenyls) or a combination of DDT (1,1,1-trichloro-2,2-bis (p-chlorophenyl) ethane), DDD (1,1-dichloro-2,2-bis (p-chlorophenyl) ethane) and DDE (1,1-dichloro-2,2,-bis (p-chlorophenyl ethylene) on organ weights, liver storage of vitamin A and carotene, selected blood chemistry parameters, and serum protein fractions were determined in penned white pelicans (Pelecanus erythrorhynchos) receiving a daily dosage of these compounds. Birds received 100 mg of PCBs or a combination of DDT (20 mg), DDD (15 mg), and DDE (15 mg) injected into the first fish fed each day for ten weeks. A greater percentage of PCB treatment was retained in brain, liver, carcass and feathers than the percentage of DDT + DDD + DDE treatment. Liver weight as percent of body weight decreased (p less than 0.01) in DDT + DDD + DDE-treated birds and increased (p less than 0.01) as a total weight in PCB-treated birds. Spleen weight as percent of body weight was greater (p less than 0.05) in PCB-treated birds. Neither treatment had a significant effect on the weight of the brain, heart, or kidney. Liver vitamin A levels were greater (p less than 0.01) on a mug/g of liver basis in the DDT-treated birds than in controls. Significant lowering of serum potassium and protein values was noted in both the PCB- and the combination of DDT, DDD, DDE-treated birds, while serum calcium values were lowered (p less than 0.01) only in PCB-treated birds. Vaues of serum inorganic phosphorus, uric acid and magnesium were not significantly changed by either treatment. Globulin fractions were unaltered by either treatment, but albumin fractions were lowered (p less than 0.01) in the PCB-treated pelicans.
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PMID:Physiological effects of polychlorinated biphenyls or a combination of DDT, DDD, and DDE in penned white pelicans. 81 Nov 79

The hematopoietic disregulation in adult mice induced by the malignant histiocytosis sarcoma virus (MHSV) and the Harvey murine sarcoma virus (Ha-MuSV), which both possess c-Ha-ras-related oncogenic sequences, was investigated. Spleen focus formation induced by MHSV and Ha-MuSV was not restricted by the Fv-2 resistance locus in congenic DDD and C57BL/6 mice, unlike leukemogenesis induced by Friend virus, Rauscher virus, and the myeloproliferative sarcoma virus (MPSV). C57BL/6 mice were much more resistant to MHSV and Ha-MuSV-induced spleen focus formation than DDD mice regardless of their Fv-2 state. Infection of DDD mice with MHSV caused a systemic histiocytic neoplasia, best described as murine malignant histiocytosis. Transformed histiocytic cells proliferated excessively in the bone marrow, spleen, and lymph nodes and, in the final stages of the disease, in all major parenchymal organs. The Ha-MuSV caused a strikingly different benign histiocytic tumor in DDD mice and, unlike MHSV, did not induce a rapid, progressive splenomegaly in C57BL/6 mice. Infection of DDD mice with MHSV induced a rapid and synchronized depletion of early and late erythroid precursor cell pools. In MHSV-infected C57BL/6 mice comparable changes were observed with dissimilar kinetics. Macrophage colony-forming cells of MHSV-infected mice were increased in number and proliferated independently of stimulating growth factors. The disease induced by MHSV in mice can thus serve as a model for malignant histiocytosis in humans.
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PMID:Murine retrovirus-induced malignant histiocytosis, an experimental model for the disease in humans. 282 12

Cellular and humoral immune responses to Pneumocystis carinii were investigated. ICR and DDD mice were intranasally infected with 10(4) mouse lung-derived P. carinii, and the delayed-type hypersensitivity (DTH) reaction and antibody titers to P. carinii were measured along with the number of P. carinii cysts in the lungs after infection. The number of P. carinii cysts in the lungs peaked at 2 weeks after infection and then decreased to barely detectable levels by 4 weeks. Serum antibody (immunoglobulin G) titers measured by indirect immunofluorescence increased up to 4 weeks. The DTH footpad reaction was most prominent at 2 weeks postinfection and declined thereafter. Thus, the decline in the number of P. carinii cysts in the lungs corresponded well with the time of the peak of the DTH reaction but not with the serum antibody response. Spleen T cells from infected mice mediated the DTH reaction when transferred intravenously into normal recipients and reduced the number of P. carinii cysts in the lungs when transferred intravenously into P. carinii-infected mice. The results indicated that cellular immunity is important for protection from subclinical P. carinii infections.
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PMID:Cellular and humoral immune responses of mice subclinically infected with Pneumocystis carinii. 387 26