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J L Pace

Publications and source records attributed to J L Pace.

72 records · Page 4Linked to original sources
PubMed1978

Specific antigens of chicken thymus.

Purified plasma membranes from chicken thymus and bursa cells were prepared and solubilized with sarkosyl (sodium salt of N-methyl-N-(1-oxodecyl)-glycine). Antisera to solubilized thymus plasma membrane (TPM) were produced in rabbits and the globulin fraction obtained by ammonium sulfate precipitation. Four precipitating antigens were detected in solubilized TPM by immunoelectrophoresis. Following absorption with chicken serum and bursa plasma membrane (BPM) immunosorbents, three antigens, designated T1, T2, T3, were specific for the TPM fraction, and one antigen, T1, was found in soluble extracts of thymus tissue. Absorption with isolated plasma membrane and whole cells indicated that the T1 and T2 antigens in solubilized TPM are associated with the plasma membrane but not expressed on the surface of the cell. A common antigen, designated BT, was detected in BPM and TPM fractions and in membrane preparations of spleen. The antigens were not detected in any other tissues or cells including brain, circulating lymphocytes and erythrocytes.

Animals↗
PubMed1975

Urticaria and hyperthyroidism.

A thyrotoxic patient presented with urticaria and this appeared to respond to beta-blockade with practolol. Symptoms did not recur when radioactive iodine treatment took effect in spite of stopping the beta-blocker. Possible mechanisms are discussed and it is stressed that more emphasis should be placed on this association.

Adult↗
PubMedDate not supplied

Expression of the interferon-gamma receptor gene in mouse placentas is related to stage of gestation and is restricted to specific subpopulations of trophoblast cells.

In order to evaluate the potential of placental cells to bind the multifunctional cytokine, interferon-gamma (IFN-gamma), tissues collected from pregnant Swiss mice were analysed for IFN-gamma receptor (IFN-gamma R) mRNA and protein. Northern blot hybridization studies indicated that the relative abundance of IFN-gamma R mRNA increased as gestation progressed to term. Analysis by in situ hybridization revealed that trophoblast cells first contained high steady state levels of IFN-gamma R mRNA at g.d. 12. At g.d. 12 and 14, transcription was restricted to cells in the spongiotrophoblast region and nests of similar cells in the labyrinthine region. These cells also contained immunoreactive IFN-gamma R protein. By g.d. 18, IFN-gamma R mRNA was clearly detectable in large spongiotrophoblast cells and labyrinthine trophoblast. IFN-gamma R mRNA was low to absent in giant trophoblast cells at all stages of gestation. Specific mRNA was present in parietal and visceral yolk sac cells by g.d. 14. Thus, expression of the IFN-gamma R gene in mouse placental cells is influenced by stage of gestation, cell lineage and state of differentiation. Whether or not these cells respond vigorously to IFN-gamma with induction of antiviral proteins, increased MHC class I antigens and growth modulation may therefore be determined by their expression of specific receptors for this pluripotent cytokine.

Allantois↗
PubMedDate not supplied

Trophoblastic cell lines generated from tumour necrosis factor receptor-deficient mice reveal specific functions for the two tumour necrosis factor receptors.

In mice and humans, expression of the tumour necrosis factor receptor-1 (TNF-R1) gene in placental trophoblast cells is constitutive whereas expression of the TNF-R2 gene is developmentally programmed. In order to study the individual functions of TNF-R1 and -R2 in this lineage, cell lines were generated from placental explants of homozygous matings of gestation day 10 outbred mice (Swiss-Webster), TNF-R1-deficient (TNF-R1-/-) and TNF-R2-/- transgenic mice as well as the background strain for the TNF-R2-/- mice (WT, C57BL/6x129). All of the cells exhibited trophoblast markers; they contained cytokeratin intermediate filaments, expressed alkaline phosphatase activity and displayed transferrin receptors, but were negative for vimentin filaments and the macrophage marker, F4/80. Analysis of DNA by polymerase chain reaction demonstrated the expected TNF-R genotype in each line. In experiments testing the effects of recombinant mouse TNF-alpha (rmTNF-alpha) on viability and proliferation of the cell lines, rmTNF-alpha modestly but dose-dependently inhibited the growth of WT and TNF-R2-/- cells while having no effect on TNF-R1-/- cells. Actinomycin D-treated WT and, to a lesser extent, TNF-R2-/- cells, were more sensitive to growth inhibition than untreated cells whereas TNF-R1-/- cell responses remained unchanged. These data indicated that rmTNF-alpha inhibits growth of trophoblastic cells through TNF-R1 and that newly synthesized protein(s) provide partial protection against toxicity. In contrast to the receptor species-specific effects on cell growth exerted by rmTNF-alpha, both TNF-R mediated inhibition of alkaline phosphatase activity. Collectively, the observations support the postulate that receptor expression is the key factor which determines the nature and extent of TNF-alpha effects on trophoblast cell growth and function.

Alkaline Phosphatase↗