Showing papers on "Receptor expression published in 1978"

Fc-Receptors on Human T Lymphocytes I. Transition of Tγ to Tµ Cells

Abstract: T lymphocytes of 11 healthy humans were enriched and studied for Fc-IgG or Fc-IgM receptor expression by using a rosette technique, namely bovine red cells coated with rabbit IgG {EA-IgG} or IgM {EA-IgM}. Eighty percent (±9.2) of the T cells (mean ± S.D.) exhibited Fc-IgM receptors after culture (designated Tµ) and 22% (±9.4) expressed Fc-IgG receptors (designated Tγ), the latter occasionally decreasing after culture at 37°C. The two populations could be readily separated by interaction of Tγ cells with EA-IgG and Ficoll-Hypaque gradient separation. In the interface we found T non-γ cells, which consisted of over 90% Tµ cells and about 1% Tγ cells. In the pellet an enriched Tγ cell population was found, 79% (±8). After lysis of the bound EA-IgG, incubation of the cells at 37°C led to capping, endocytosis, and/or shedding of the Fc-IgG receptor. Culture of these cells led to expression of Fc-IgM receptors on these originally Tγ cells, whereas only a few cells re-expressed Fc-IgG receptors. The transition of Tγ → Tµ cells was also observed in T cells precultured for 24 hr and required immune complex (IC) interaction. Adding sodium azide or maintaining the cells at 4°C blocked Fc-IgM receptor expression. X-irradiation, cytochalasin B, and colchicine had no effect. Pronase treatment of positively selected Tγ cells uncovered Fc-IgG receptors, which did not cap, and after 40 hr in culture, T cells bearing Fc-IgG and Fc-IgM receptors were found. Therefore, Fc-IgG and Fc-IgM receptors do not appear to be markers for distinct T cell subsets under some conditions. Rather, a subset of T cells may conceivably express both classes of receptors at different functional stages. The interaction of Fc-IgG receptors with IC may serve to alter the overall expression of Fc-receptors.

Assignment of the receptor for ecotropic murine leukemia virus to mouse chromosome 5

Abstract: The gene for the receptor for ecotropic murine leukemia virus (Rev) has been assigned to mouse chromosome 5. This determination was made possible by an analysis of somatic cell hybrids between mouse and Chinese hamster cells. The parents of these hybrids were A/HeJ or Mus poschiavinus peritoneal exudate cells or BALB/c primary embryo fibroblasts and E36, a Chinese hamster lung fibroblast deficient in hypoxanthine guanine phosphoribosyltransferase. Segregation of mouse chromosomes in these hybrids was analyzed by chromosome banding and isozyme expression. Cells were tested for their ability to absorb and replicate vesicular stomatitis virus (murine leukemia virus [MuLV]) pseudotype particles and ecotropic MuLV as measured by the XC test. The presence of chromosome 5 was essential for receptor expression as determined by three statistical procedures. Segregation of the receptor for ecotropic murine leukemia virus was also followed in two series of subclones. In both, receptor expression was syntenic with phosphoglucomutase-1, an isozyme which has been mapped to mouse chromosome 5.

Relationship between Epstein-Barr virus (EBV)-production and the loss of the EBV receptor/complement receptor complex in a series of sublines derived from the same original Burkitt's lymphoma.

Abstract: Virus production, EBV (P3HR-1 substrain) superinfectability, IdUrd inducibility, EBV receptor and complement (C3) receptor expression were assessed in two independently maintained jijoye lines, the derived P3HR-1 clone that releases a growth inhibitory and cytopathic, non-transforming viral mutant, and in non-producer sublines derived from the P3HR-1 line by the spontaneous cessation of virus production. Both jijoye lines were superinfectable, inducible, and carried EBV and C3 receptors. Virus-producing P3HR-1 cells and recently derived non-producer sublines lacked EBV-receptors and C3 receptors, could not be superinfected, but were IdUrd inducible. Two long-passaged, non-producer sublines of P3HR-1 reexpressed EBV and C3 receptors to an equal degree (different in the two sublines). EBV-superinfectability became partially reestablished in the subline with the higher expression of EBV and C3 receptors. These findings support the hypothesis that the EBV-receptor/C3 receptor negativity of the producer P3HR-1 sublines and their recent non-producer derivatives is due to negative selection by the growth-inhibitory, cytopathic P3HR-1 virus variant. The closely linked disappearance and reappearance of EBV-receptors and complement receptors gives further support to the idea that these two receptors are either identical or closely linked constituents of the cell membrane.

Fc-IgM and Fc-IgG receptors on human circulating B lymphocytes.

Abstract: Peripheral blood B cells from normal humans were enriched with rosette techniques (mean 93.5% surface immunoglobulin positive). We studied these purified B cells for the expression of Fc-IgG and Fc-IgM receptors by using bovine red blood cells coated with IgG (EA-IgG) or IgM (EA-IgM). Between 81 and 94% (mean 88.67%) Fc-IgG and between 79 and 97% (mean 87.5%) Fc-IgM receptor positive cells were found by using this sensitive rosette technique. The Fc-IgG receptor values had a tendency to decrease in culutre at 37°C. In contrast, cultivation at 37°C for 24, 48, and even 72 hr enhanced Fc-IgM receptor expression. Trypsinization (0.25%) removed Fc-IgM receptors, but not Fc-IgG receptors. However, after further cultivation of the trypsinized cells, Fc-IgM receptors were re-expressed on the same or even greater percentages of cells. Fc-IgM receptors were also detected on monoclonal B cells (chronic lymphatic leukemia cells) expressing surface immunoglobulins with either δ or γ heavy chains exclusively. The high percentage of Fc-IgM positive cells in normal peripheral blood B cells, coupled with the observation that the Fc-IgM receptors are not confined to monoclonal B cells with particular classes of surface immunoglobulins, suggests that the Fc-IgM receptor may be present on essentially all B cells. Moreover, our results suggest that most human B cells expressed both Fc-IgM and Fc-IgG receptors simultaneously.

Surface morphology of bone marrow lymphocytes. I. Scanning electron microscopy of small lymphocytes bone marrow and spleen

Abstract: Cell separation techniques and scanning electron microscopy (SEM) were used to characterize the surface morphology of small lymphocytes in mouse bone marrow. Lymphocyte-rich fractions and unfractionated suspensions of bone marrow and spleen cells from 9--10-week-old C3H male mice were glutaraldehyde-fixed, syringed onto gelatin-coated silver membranes, dehydrated in ethanol, infiltrated with amyl acetate, critical point dried, coated with gold-palladium and examined by SEM. High proportions of cells were retained on the membranes. Purified spleen small lymphocytes showed unimodal distribution curves for cell diameter (mode, 3.4 micrometer) and for number of surface microvilli (mode, 55--60). Bone marrow small lymphocytes were identified initially in lymphocyte-rich marrow fractions and in erythroblast-depleted marrow from polycythemic mice as well as in normal whole marrow. The cells resembled spleen small lymphocytes in size distribution and they showed microvilli. However, the number of visible microvilli was lower on small lymphocytes in the bone marrow (mode, 35--40) than in the spleen. While in each small lymphocyte population the total number of microvilli was greater on larger cells than on smaller ones, the density of microvilli per unit area of cell surface tended to decrease with increasing cell size. The results establish that the small lymphocytes in mouse bone marrow, mainly locally-produced immature cells, have villous surfaces, but the number of microvilli per unit cell surface area is less than that on peripheral small lymphocytes, as seen in the spleen. Neither in the bone marrow nor in the spleen are subpopulations of small lymphocytes distinguishable solely by numbers of microvilli. The findings suggest that microvilli on bone marrow small lymphocytes may undergo further development during post-mitotic maturation, surface receptor expression and migration of the cells to peripheral lymphoid tissues.