PROLIFERATION OF B AND T CELLS IN MIXED LYMPHOCYTE CULTURES

Electrophoretically fractionated CBA/Ca spleen T cells alone respond to allogeneic cells in one-way MLC and to PHA. They do not respond to E. coli LPS. B cells alone do not respond to allogeneic cells nor to PHA, but do respond to LPS. When karyotypically distinguishable syngeneic mixtures of T and B lymphocytes are stimulated with allogeneic cells, at the most 5% of mitoses on 5–9th culture day are of B cell origin. This indicates that B cells are not substantially recruited to proliferate in the MLC

Distribution of the major histocompatibility complex antigens in human and rat kidney

Distribution of the major histocompatibility complex antigens in human and rat kidney. We have compared the distribution of the major histocompatibility complex (MHC) antigens in human and rat kidney using monospecific antisera to class I and II antigens of the MHC. FITC/TRITC double immunofluorescence was used to demonstrate these antigens in frozen sections and the Staphylococcus aureus Cowan I rosette assay on the cell surface. In both species, the MHC antigens were prominently present on the passenger leukocytes. Immunofluorescence analysis of human kidney demonstrated that the class I, β2-microglobulin (β2m), and class II antigens were present in the vascular endothelial cells and class I antigens in the renal tubular cells. The Staphylococcus assay demonstrated that these antigens were also exposed on the respective cell surfaces. In clear contrast, in the rat, class I, the β2m, and class II antigens were absent from the kidney vascular endothelium of large vessels and intertubular capillaries; however, large amounts of class II antigens were seen inside the proximal renal tubular cells. The Staphylococcus assay indicated that none or very little of these antigens were exposed on the kidney parenchymal cell surface. These differences may explain why rat renal transplants are relatively non-immunogenic and easily accepted, whereas human renal transplant recipients must be immunosuppressed ad infinitum.Distribution des antigènes du complexe d'histocompatibilité principal du rein d'homme et de rat. Nous avons comparé la distribution des antigènes du complexe d'histocompatibilité principal (MHC) dans du rein d'homme et de rat en utilisant des antisérums monospécifiques des antigènes des classes I et II du MHC. Une double immunofluorescence FITC/TRITC a été utilisée pour démontrer ces antigènes dans des sections congelées et le dosage des rosettes de Staphylocoque doré Cowan I pour les démontrer à la surface cellulaire. Dans les deux espèces, les antigènes MHC étaient essentiellement présents sur les leucocytes de passage. L'analyse en immunofluorescence de rein humain a démontré que les antigènes de classe I, 1 β2-microglobuline (β2m) et de classe II étaient présents dans les cellules endothéliales vasculaires, et ceux de classe I dans les cellules tubulaires rénales. Le dosage Staphylocoque a démontré que ces antigènes étaient également exposés sur les surfaces cellulaires respectives. De facon clairement opposée, chez le rat, les antigènes de classe I, 1 β2m et de classe II étaient absents de l'endothélium vasculaire rénal des gros vaisseaux et des capillaires intertubulaires; cependant, de grandes quantités d'antigènes de classe II étaient visibles à l'intérieur des cellules tubulaires rénales proximales. L'essai Staphylocoque a indiqué qu'aucun ou très peu de ces antigènes étaient exposés à la surface des cellules parenchymateuses rénales. Ces différences pourraient expliquer pourquoi les greffons rénaux de rat sont relativement non immunogènes et facilement tolérés, alors que les receveurs de transplants rénaux humains doivent être immunodéprimés indéfiniment

Characterization of surface glycoproteins of mouse lymphoid cells

We have labeled exposed surface glycoproteins of mouse lymphoid cells by the galactose oxidase-tritated sodium borohydride technique. The labeled glycoproteins were separated by polyacrylamide slab gel electrophoresis and visualized by autoradiography (fluorography). The major thymocyte surface proteins have molecular weights of 170,000 and 125,000. Thymocytes from TL antigen-positive mouse strains showed an additional band with a molecular weight of 27,000. Highly purified T lymphocytes contain two major surface glycoproteins with molecular weights of 180,000 and 125,000. Purified B lymphocytes have one major surface glycoprotein with a molecular weight of 210,000. When T lymphocytes are stimulated in vitro by concanavalin A or phytohemagglutinin, the major proteins characteristic of T cells are relatively weakly labeled, but new components of lower molecular weights appear on the cell surface. A similar change is seen in B lymphocytes stimulated by Escherichia coli lipopolysaccharide. T lymphoblasts isolated from mixed lymphocyte cultures show a slightly different surface glycoprotein pattern. A polypeptide with a molecular weight of 57,000, which was labeled without enzymatic treatment by tritiated sodium borohydride alone, is strongly labeled in proliferating cells

Cytomegalovirus infection of human kidney cells in vitro

Cytomegalovirus infection of human kidney cells in vitro. To study which structures of a kidney allograft are the main targets for cytomegalovirus (CMV), human glomerular epithelial and mesangial cells, as well as tubular epithelial and endothelial cells were isolated by steel meshes of different pore sizes and enzymatic treatments. The various cultured cell types were characterized by morphology and specific antibodies. Human CMV was inoculated onto cell monolayers using two different culture methods: conventional tissue culture and rapid shell vial culture. To analyze whether CMV had a direct effect on the immunologic properties of kidney parenchymal cells, MHC class I and class II antigen expression was estimated before and after the infection. CMV infected all kidney cells identically. All cells expressed class I strongly after the infection, but they were class I positive prior to infection. Class II antigens were not expressed on the cell surface either before or after the infection. In conclusion, human kidney cells of glomerular, tubular and vascular origin were all infected by CMV without any difference. CMV had no significant direct effects on the antigenic properties of the cells