TRANSFORMATION OF A HISTOCOMPATIBILITY IMMUNOGEN INTO A TOLEROGEN

H-2 antigens on spleen cell membranes absorb antibody to H-2 antigens and induce both humoral and cellular responses. Liver cell membrane H-2 antigens by contrast also absorb antibody but do not influence cellular response and are tolerogenic for the humoral response. This paper demonstrates that syngeneic liver cells contain a substance which can transform the properties of allogeneic spleen cell membranes into those of allogeneic liver cell membranes, i.e., transform a humoral immunogen into a humoral tolerogen. The process appears to be accompanied by cleavage of an antigen component from the spleen membrane and hence to result in a structural change in the H-2 antigen.

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Permeability of the liver cell membrane to quinolinate

Biochemical Journal ◽

10.1042/bj1640283 ◽

1977 ◽

Vol 164 (1) ◽

pp. 283-286 ◽

Cited By ~ 5

Author(s):

K R F Elliott ◽

C I Pogson ◽

S A Smith

Keyword(s):

Steady State ◽

Cell Membrane ◽

Guinea Pig ◽

Liver Cell ◽

Liver Cells ◽

Pig Liver ◽

Liver Cell Membrane ◽

Guinea Pig Liver

Quinolinate was taken up by both rat and guinea-pig liver cells. Equilibrium was reached after approx. 20 min with rat cells, but guinea-pig cells had not achieved a steady state after 60 min. There was no evidence to suggest that quinolinate is rapidly metabolized by either species. The concentrations of quinolinate attained in rat and guinea-pig cells after short periods of incubation with 0.5 mM-quinolinate did not inhibit gluconeogenesis. These results raise further doubts as to the mechanism of quinolinate action in liver.

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Studies on the Function of Cell Membrane 9th Report: Protective Action of Sodium Taurine N-Carbo-Dithioate (TDT) Against CCl4-Induced Biochemical Changes in Liver Cell Membrane of Rats

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)31524-0 ◽

1973 ◽

Vol 23 (6) ◽

pp. 773-779

Author(s):

Yasusuke MASUDA ◽

Masato KUCHII ◽

Nobuyuki OKADA ◽

Tadashi MURANO

Keyword(s):

Cell Membrane ◽

Liver Cell ◽

Protective Action ◽

Biochemical Changes ◽

Liver Cell Membrane

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Pathogenesis of shigella diarrhea. VII. Evidence for a cell membrane toxin receptor involving β1 {arrow} 4-linked N-acetyl-D-glucosamine oligomers

Journal of Experimental Medicine ◽

10.1084/jem.146.2.535 ◽

1977 ◽

Vol 146 (2) ◽

pp. 535-546 ◽

Cited By ~ 42

Author(s):

GT Keusch ◽

M Jacewicz

Keyword(s):

Cell Membrane ◽

Cholera Toxin ◽

Liver Cell ◽

Hela Cells ◽

Mammalian Cells ◽

Cell Membranes ◽

Proteolytic Enzymes ◽

Cell Monolayer ◽

Toxin Receptor ◽

Toxin Uptake

The binding of ShigeUa dysenteriae 1 cytotoxin to HeLa cells in culture and to isolated rat liver cell membranes was studied by means of an indirect consumption assay of toxicity from the medium, or by determination of cytotoxicity to the HeLa cell monolayer. Both liver cell membranes and HeLa cells removed toxicity from the medium during incubation, in contrast to WI-38 and Y-1 mouse adrenal tumor cells, both of which neither bound nor were affected by the toxin. Uptake of toxin was directly related to concentration of membranes added, time,and temperature, and indirectly related to the ionic strength of the buffer used. The chemical nature of the membrane receptor was characterized by using three principal approaches: (a) enzymatic sensitivity; (b) competitive inhibition and (c) receptor blockade studies. The receptor was destroyed by proteolytic enzymes, phospholipases (which markedly altered the gross appearance of the membrane preparation) and by lysozyme, but not by a variety of other enzymes. Of 28 carbohydrate and glycoprotein haptens studied, including cholera toxin and ganglioside, only the chitin oligosaccharide lysozyme substrates, per N-acetylated chitotriose, chitotetraose, and chitopentaose were effective competitive inhibitors. Greatest inhibition was found with the trimer, N, N', N" triacetyl chitotriose. Of three lectins studied as possible receptor blockers, including phytohemagglutinin, concanavalin A, and wheat germ agglutinin, only the latter, which is known to possess specific binding affinity for N, N', N" triacetyl chitotriose, was able to block toxin uptake. Evidence from all three approaches indicate, therefore, existence of a glycoprotein toxin receptor on mammalian cells, with involvement of oligomeric β1{arrow}4-1inked N-acetyl glucosamine in the receptor. This receptor is clearly distinct from the G(M1) ganglioside thought to be involved in the binding of cholera toxin to the cell membrane of a variety of cell types susceptible to its action.

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A monoclonal antibody directed against an organ-specific liver cell membrane antigen in rabbits

Journal of Immunological Methods ◽

10.1016/0022-1759(84)90165-0 ◽

1984 ◽

Vol 68 (1-2) ◽

pp. 341-348 ◽

Cited By ~ 12

Author(s):

T. Poralla ◽

W. Dippold ◽

H.P. Dienes ◽

M. Manns ◽

K.-H. Meyer zum Büschenfelde

Keyword(s):

Monoclonal Antibody ◽

Cell Membrane ◽

Liver Cell ◽

Liver Cell Membrane ◽

Organ Specific ◽

Cell Membrane Antigen

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THE EFFECT OF INSULIN ON THE DISTRIBUTION OF GLUCOSE BETWEEN THE BLOOD PLASMA AND THE LIVER IN ALLOXAN-DIABETIC AND ADRENALECTOMIZED RATS

Canadian Journal of Biochemistry and Physiology ◽

10.1139/y63-273 ◽

1963 ◽

Vol 41 (1) ◽

pp. 2431-2439 ◽

Cited By ~ 2

Author(s):

G. Hetenyi Jr. ◽

F. K. Kopstick ◽

L. J. Retelstorf

Keyword(s):

Cell Membrane ◽

Blood Plasma ◽

Liver Cell ◽

Liver Glycogen ◽

Liver Cells ◽

Diabetic Rats ◽

Hepatic Cell ◽

Very High ◽

Adrenalectomized Rats

In diabetic rats the concentration of glucose in the liver was less than in the plasma. The relative accumulation of glucose in the liver cell after the injection of insulin was also found to be significantly less in previously untreated diabetic than in normal rats. Pretreatment with insulin restored the response to normal. Experiments with labeled glucose indicated that the rate at which glucose is carried through the hepatic cell membrane is very high compared to the rate at which glucose is being formed in the liver cells in diabetic rats. The relatively small amount of glucose accumulating after insulin in livers of diabetic rats originates from the plasma. In adrenalectomized rats which have very little liver glycogen, the relative accumulation of glucose in liver cells, following the injection of insulin, was less than that in normals. These experiments indicate that in normal rats a large part of the glucose retained in the liver after the injection of insulin originates from non-labeled endogenous hepatic sources, presumably glycogen.

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