Blood transfusion induces specific cytotoxic cells.
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Biomedical subjects
Publications and source records attributed to M J Dallman.
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In this study donor specific blood transfusion of PVG recipients prevented rejection of DA strain kidneys but, paradoxically, failed to prevent the rapid and progressive accumulation of large numbers of mononuclear cells within enhanced grafts. Morphometric analysis showed that the percentage cellular infiltrate at day 3 was significantly greater in enhanced than in rejecting grafts but a notable feature in the phenotypic analysis of day 5 infiltrates was a markedly reduced number of MRC OX8 positive cells (Tc/s and NK cells) in enhanced grafts. Both rejecting and enhanced allografts showed a marked induction not only of class I but also of class II MHC antigens, and quantitative absorption analysis of donor class I MHC antigens indicated that induction occurred more rapidly in enhanced grafts. Taken together, these findings suggest that blood transfusion sensitizes the recipient, resulting in a more rapid allograft response, but that even in the presence of massive MHC/antigen induction and large numbers of infiltrating cells, immunoregulatory mechanisms are able to suppress the rejection response.
Primary lymphosarcoma of the spinal cord has been infrequently reported. This tumor was classified as intramedullary, the least common type of spinal cord tumor. The dog had rapid onset of paresis and paralysis, with no sign of spinal pain.
We studied the potential immunoenhancing effects of high doses of rIL-2 on murine T and B cell functions in vivo. Injection of rIL-2 caused a threefold or more increase in the frequencies of antigen-specific proliferative T cells, suggesting that rIL-2 initiated a polyclonal T cell response. In primary and secondary humoral immune responses, administration of rIL-2 in vivo selectively enhanced the production of IgM antibodies, whereas the IgG response was unaffected. Coadministration of rIL-2 with antigen failed to induce an isotype switch from IgM to IgG in genetically low-responding mice. Interestingly, in mice treated with rIL-2 alone (in the absence of exogenous antigen), polyclonal IgM production was induced. Polyclonal IgM production of lesser magnitude was found when mice were immunized with specific antigen in the absence of exogenous rIL-2, suggesting that local IL-2 concentrations in a primary immune response might be sufficient to elicit a polyclonal IgM response.
Scanning electron microscopy was used to examine canine tracheal cartilage and to determine the relationship between the fibrous and amorphous matrix in this tissue. Collapsed tracheal (CT) cartilage was hypocellular, compared with normal tracheal cartilage. The amorphous matrix of CT cartilage had a porous, fissured texture and did not have the homogeneous appearance of normal tracheal cartilage. Capillaries were seen to pass through CT cartilage. Randomly distributed connective tissue fibers, evident in CT cartilage matrix, were frequently attached to irregular shapes and sizes of amorphous matrix.
A mouse monoclonal antibody, designated MRC OX-19, has been prepared that binds to virtually all rat thymocytes, T lymphocytes and a maximum of 2% B lymphocytes. Immunoperoxidase studies on tissue sections showed no reactivity with nonlymphoid cells in intestine, thymus, spleen and lymph node. The antigen recognized by MRC OX-19 antibody was identified by metabolic and cell surface labeling of thymocytes followed by immunoprecipitation and sodium dodecyl sulfate gel electrophoresis. It is a surface glycoprotein of Mr = 69 000. When included in in vitro assays for T cell functions, MRC OX-19 increased proliferation stimulated by allogeneic spleen cells or the lectins phytohemagglutinin and concanavalin A. The antibody itself was not mitogenic and its stimulatory effect could be correlated with an increase in interleukin 2 production. Taken together the data suggest that MRC OX-19 could be the equivalent of mouse Ly-1 antigen and human T1 antigen.
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Tracheas were removed from 8 average-sized (13 to 19 kg) dogs, 12 toy breed dogs, and 6 toy breed dogs with collapsed trachea. The tracheal arcs were counted whenever possible and measurements of the inner ventrodorsal and lateral diameters, lumen areas, cartilage and muscle thicknesses, and numbers of chondrocytes and muscle cells/0.1 mm2 were obtained from 3 regions. The regions were the 3rd ring caudal to the larynx, the region at the thoracic inlet, and the 2nd ring cranial to the carina. The 3 tracheal regions were compared with one another for all the variables in the 3 dog groups. All groups exhibited similar significant regional variations for tracheal diameters, lumen areas, and cartilage and muscle thicknesses. There were no significant differences between regions for chondrocyte and muscle cell counts. In the comparison of average dogs and normal toy breed dogs, the former had larger ventrodorsal tracheal diameters, lumen areas, and cartilage and muscle thicknesses. The measurements from the toy breed dogs with collapsed tracheas were smaller than those from the normal toy breed dogs. There were no significant differences in chondrocyte and muscle cell counts between average dogs and normal toy breed dogs.
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Tracheal resection and anastomosis were done on 7 dogs, and a modified procedure to provide optimum first-intention healing, minimum connective tissue proliferation, and optimum epithelialization was used. To test the integrity of the technique at high incision-line tensile forces, 15 to 17 tracheal rings were excised. Excessive tracheal manipulation resulted in an increased amount of lamina propria and submucosa collagenous tissue, increased size and number of blood vessels, and increased leukocytic invasion. Criteria for a successful anastomosis were minimum postoperative coughing, good mucosal apposition and epithelialization, and tracheal lumen diameters that were at least 80% of the preoperative measurement.
The induction of polyarthritis in rats by intradermal immunisation with homologous or heterologous type II collagen incomplete or incomplete Freund's adjuvant was reported recently by Trentham et al. We have now produced a similar disease in certain strains of mice.
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Examinations were made of three sections of trachea obtained from eight dogs. The sections examined were at the regions of the second ring caudal to the larynx, the thoracic inlet, and the origin of the brachiocephalic trunk. Measurements were made of the lateral and ventrodorsal diameters, the lumen area of the trachea, the width and thickness of the tracheal cartilages, and the thickness of the trachealis muscle. Cell counts-per-square-micrometer of the cartilage and trachealis muscle were made. The results of these measurements were subjected to statistical analyses by means of one-way and two-way analyses of variance. The tracheal diameters, cartialge thickness, muscle thickness, and tracheal lumen area had significantly different measurements among the areas compared with both statistical methods. Ventrodorsal tracheal diameter and lumen area were not found to have significantly different measurements between the levels of the thoracic inlet and the brachiocephalic trunk. The cell counts did not have significantly different values among the areas considered when body weight was not a factor, but the values were significant when weight was a factor.
Experimental ethylene glycol toxicosis in dogs produced a marked increase in serum osmolality. By comparing measured and calculated serum osmolality and relating this difference to plasma ethylene glycol, it was determined that ethylene glycol was primarily responsible for the hyperosmolemia. Osmometry may provide a useful adjunct to other diagnostic tests in identifying ethylene glycol intoxicated dogs during the early, most treatable, stage of toxicosis.