Subpopulation Of Mice Research Articles

Antibody directed against Friend leukemia virus stimulates DNA synthesis in a subpopulation of mouse B lymphocytes.

Goat and rat antisera directed against Friend leukemia virus (anti-FLV) were found to be B-lymphocyte mitogens stimulating DNA synthesis in these cells but not in T lymphocytes. Membrane fluorescence microscopy showed that anti-FLV reacts with a subset of B lymphocytes of which the majority express immunoglobulin mu chains. The mitogenic effect was found with all mouse strains tested including 129 and AKR. Absorption experiments with purified viruses indicated that the mitogenic effect is specific for an antigen present in murine leukemia viruses of the FMR subgroup. In absorption experiments with viable cells, the antigen involved in mitogenicity was found to be expressed on Friend erythroleukemia cell lines (4/4) and on myelomas (2/2) but not on normal thymus T lymphomas (0/2) or on rabbit or mink cells infected with BALB/c xenotropic virus. Preincubation of spleen cells with anti-gp70 antiserum inhibited the mitogenic effect of anti-FLV but not of lipopolysaccharide.

Peanut Agglutinin

Peanut agglutinin (PNA) has previously been shown to be a 'marker' for early T subpopulations in mice. We have investigated whether it could also be used in the study of human mononuclear cells. 50--60% of human thymocytes have binding sites for PNA. When separated on a discontinuous Ficoll gradient, the PNA-positive thymocytes are found preferentially in the layers corresponding to the immunoincompetent cells. In the peripheral blood only 5% of the mononuclear cells are PNA-positive and we have shown that these cells are monocytes. In tonsils 13% of PNA+ cells are found and they are mostly lymphocytes. Thus, PNA is a marker for some T cell subsets present in the thymus and tonsils.

Depression of cytotoxic T cell subpopulation in mice by hydrocortisone treatment

Immunization with allogeneic DBA/2 mastocytoma cells produced a decrease in thymic size and number of thymus cells and an increase in spleen size and number of spleen cells. The cells that remained in the thymus were more capable of inducing a graft-versus-host (GVH) reaction than thymus cells from untreated mice. Similar results were found if mice were treated with hydrocortisone. Hydrocortisone treatment before or after immunization with DBA/2 mastocytoma decreased the number and/or the activity of killer cells. Lymphocytes with killer cell activity against an allogeneic tumor were a different subpopulation of T cells than those that induced a GVH reaction. These results suggest that killer lymphocytes originate from precursor cells in the cortex of the thymus, are mobilized to the peripheral lymphoid tissues after immunization by mastocytoma cells, and are sensitive to hydrocortisone treatment. The mobilized lymphocytes are most likely incompletely differentiated cells of the killer lymphocyte class (T 1). Our results, however, did not prove that hydrocortisone sensitivity of these cells is related to their immaturity. Probably, there are at least two separate subpopulations of lymphocytes in the thymus: (a) T 2 cells (mature T), located in the medulla, that have vigorous capacity to induce GVH reaction, and (b) T 1 cells located in the cortex (incompletely differentiated), which need an additional maturation step to become mature T 2 cells: among these cells are those that become killer T-lymphocytes.