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H Kolb

Publications and source records attributed to H Kolb.

At least 325 records · Page 18Linked to original sources
PubMed1982

Low-dose streptozotocin-induced autoimmune diabetes is under the genetic control of the major histocompatibility complex in mice.

In mice, an experimental autoimmune diabetes can be induced by multiple injections with low doses of streptozotocin. Since different mouse strains show a varying susceptibility towards this treatment, we have examined whether the experimental autoimmune diabetes is under the genetic control of the major histocompatibility complex (H-2 complex). Mice of five congenic resistant strains, differing in their genome only at the H-2 region, were identically treated on five consecutive days with 40 mg streptozotocin/kg body weight. Genes at the H-2 complex were found to determine the susceptibility towards the diabetogenic effect of streptozotocin: mice of H-2 haplotype k (B10.BR) developed persistent and strong hyperglycaemia (blood glucose approximately 17 mmol/l), mice of strain B10.A (H-2a), C57BL/10 (H-2b) and B10.D2 (H-2d) reacted with moderate hyperglycaemia (between 11.5 and 15.5 mmol/l), whereas mice of strain B10.S (H-2s) were resistant to the diabetogenic effect of low-dose streptozotocin except for a small and transient rise of blood glucose levels. It is concluded that genes within the major histocompatibility complex affect the diabetogenic response to multiple low-dose streptozotocin treatment.

Animals↗
PubMed1982

A-type horizontal cells of the superior edge of the linear visual streak of the rabbit retina have oriented, elongated dendritic trees.

The horizontal cells of the rabbit retina have been studied by light microscopy of Golgi-impregnated whole-mount retinas. The two types of horizontal cell of the rabbit retina are similar to the horizontal cells of the cat retina in most respects. However, the majority of the A-type horizontal cells of the rabbit have asymmetrical dendritic fields compared to the circular, symmetrical dendritic fields of this cell type in the cat. The A-type horizontal cells of the superior edge of the linear visual streak in the rabbit retina are the most strikingly asymmetric and most of them are elongated and oriented in a direction approximately parallel to the linear visual streak. Like H1 axon terminals of the turtle retina the oriented, elongated A-type horizontal cells of the rabbit visual streak region may play a role in the neurocircuitry which underlies orientation sensitive ganglion cells.

Animals↗
PubMed1982

Electron microscopic evidence for an asialoglycoprotein receptor on Kupffer cells: localization of lectin-mediated endocytosis.

Direct evidence is given for the presence of an N-acetyl-D-galactosamine-specific lectin on the Kupffer cell surface by visualization of ligand binding in electron microscopy. When freshly isolated Kupffer cells are incubated with asialofetuin adsorbed onto colloidal gold particles (ASF-gold), binding and endocytosis of ligand are seen. Recognition of ASF-gold by Kupffer cells is completely abolished in the presence of N-acetyl-D-galactosamine (25 mM) or EGTA (3 mM), but is not significantly reduced by N-acetyl-D-glucosamine or D-mannose (25 mM). ASF particles are endocytosed via the coated pit/vesicle pathway and appear to be transported to the secondary lysosomes by coated vesicles, as shown by the occurrence of coated areas in the secondary lysosome membrane. These observations demonstrate the presence of an asialoglycoprotein receptor on Kupffer cells; therefore, the hepatocyte is not the only cell in the rat liver with D-galactose receptor activity.

Animals↗
PubMed1981

Does the D-galactose receptor on Kupffer cells recycle?

Kupffer cells carry on the cell surface a lectin-like receptor with specificity for D-galactose/D-glucose residues. After tryptic digestion of receptors, new lectin activity appears on the plasma membrane within 15 min. Protein biosynthesis de novo is not involved. This indicates the transfer of new lectin molecules stored within the cell to the cell surface. Kupffer cells can enter a physiological state where receptor recycling does not take place.

Animals↗
PubMed1981

Induction of experimental autoimmune diabetes by low-dose streptozotocin treatment in genetically resistant mice.

We have studied the effect of suppressor cell elimination on the induction of experimental autoimmune diabetes in mouse strains which are normally low or intermediate responders to multiple low-dose streptozotocin treatment. BALB/c (low responder) and C57BL/6J (intermediate responder) mice received 70 mg cyclophosphamide/kg, 1 or 6 days before the onset of streptozotocin injections. Following cyclophosphamide treatment, BALB/c mice become susceptible to the diabetogenic effect of streptozotocin. Similarly the manifestation of diabetes in C57BL/6J mice is enhanced. Thus in both strains immunomodulation by cyclophosphamide treatment significantly increases the susceptibility towards the diabetogenic effect of streptozotocin. We therefore conclude that in mice of strains BALB/c and C57Bl/6J suppressor cells control the level of resistance towards the induction of experimental autoimmune diabetes by low-dose streptozotocin treatment.

Animals↗
PubMed1981

Lectin mediates homing of sialidase-treated erythrocytes of the liver as revealed by scintigraphy.

Mammalian erythrocytes loose their normal circulatory pattern following desialylation by sialidase and are trapped in the liver. The mechanism responsible for this phenomenon has been studied by a new scintigraphic method. We report here that the retention of asialo-erythrocytes in the liver is due to the interaction between a lectin-like receptor on Kupffer cells and terminal D-galactosyl residues exposed on erythrocytes after sialidase treatment. The major findings supporting the conclusion are: First, kinetics of asialo-erythrocyte accumulation in the liver are identical in conventional and germfree animals, demonstrating that the presence of serum antibody is not essential. Second, trapping of asialo-erythrocytes can be substantially inhibited by intravenous injection of N-acetyl-D-galactosamine or galactosylated bovine serum albumin, other saccharides or glycoproteins are less or not at all effective. This specificity pattern is characteristic for the D-galactose-specific lectin on Kupffer cells. It therefore appears that the retention of sialidase-treated erythrocytes in the liver is lectin- and not antibody mediated.

Animals↗
PubMed1981

Strain dependency of the transfer of experimental immune insulitis in mice.

Multiple treatment with low doses of streptozotocin induces hyperglycaemia with concomitant lymphocytic infiltrations into pancreatic islets (insulitis) in several mouse strains. The transfer of cellular immune reactions against islet cells by means of spleen cells was tested in two congeneic and five allogeneic strain combinations. Donor mice were treated on 5 consecutive days with 40 mg streptozotocin per kg body weight. Three weeks later, 5 x 10(7) live spleen cells were transferred into thymusless recipient mice. Insulitis which had developed in about 70% of the donors was only transferable from C57B1/6J to congeneic thymusless mice. In a second congeneic and in all allogeneic strain combinations, cellular immune reactions against pancreatic islets could not be transferred. In none of the recipients of spleen cells from diabetic donors was hyperglycaemia observed. As streptozotocin-induced cellular immune reactions against pancreatic islet cells were only transferable in one congeneic and in no allogeneic strain combinations, it is concluded that there is a genetic restriction both on the levels of donor and recipient mice.

Animals↗
PubMed1981

Cellular immune reactions against pancreatic islets as a consequence of graft versus host disease.

We studied autoimmune reactions against pancreatic islets occurring as a consequence of defects of the immune system rather than after pathological changes in the endocrine organ itself. Immune dysregulation was induced by transfer of parental lymphocytes into semi-allogeneic F1 recipient mice (graft versus host reaction, GVHR). Recipients were killed 1 month after the induction of the disease. Pancreatic islets were screened by light microscopy for signs of lymphocytic infiltration (insulitis). Severe insulitis was found in all mice undergoing GVHR. The cytotoxic activity of lymphocytes was apparent in electron microscopic studies and affected only B cells. Infiltrations were not seen in the exocrine part of the pancreas nor in heart, liver or kidneys at this early stage of GVHR. It is concluded that non-specific disorders of the immune system induced by GVHR may lead to specific cellular autoimmune reactions against B cells of pancreatic islets.

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