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S Marshall-Clarke

Publications and source records attributed to S Marshall-Clarke.

At least 37 records · Page 2Linked to original sources
PubMed1986

Concanavalin A-stimulated rat spleen cells produce a soluble factor that supports growth of the mouse IL-3-dependent cell line Ea3.123, but not three other IL-3-dependent lines.

Several cloned, non-leukaemic mouse haemopoietic cell lines are believed to be uniquely dependent on interleukin-3 (IL-3) for their survival. All of these lines require the addition of WEHI-3B cell-conditioned medium for their growth. We have examined the growth requirements of four IL-3-dependent cell lines and found that only one, Ea3.123, is able to grow in medium conditioned by concanavalin A-stimulated rat spleen cells (rat ConACM), whereas the other three, AC2, 32D cl-23 and FDC-P2, are not. Medium conditioned by the growth of concanavalin A-stimulated mouse spleen cells (mouse ConACM) supports the growth of all four cell lines. The Ea3.123-supporting activity in rat ConACM appears to be of smaller size (approximately 27,000) than the activity in mouse ConACM and WEHI-3BCM (approximately 38,000). The activity is unlikely to be due to GM-CSF, since post-endotoxin serum containing GM-CSF does not support growth of Ea3.123, nor is it likely to be IL-2, since we were able to remove IL-2 by absorption with CTLL-16 cells without affecting the ability of rat ConACM to support Ea3.123 cells. Our findings have important implications for the assay of IL-3, and mechanisms by which dependent cells respond to IL-3.

Animals↗
PubMed1986

Transformation induced by Echinococcus granulosus protoscoleces in unprimed murine spleen cells: identity and MHC restriction of participating cell types.

Transformation induced by Echinococcus granulosus in unprimed murine spleen cells in vitro was not prevented by rigorous T- or B-cell depletion. When naïve T- or B-cell populations were further depleted of macrophages, B-cell transformation was relatively unaffected whereas T-cell transformation was totally inhibited. Peritoneal macrophages from infected mice could present a mitogenic stimulus to purified, naïve T-cells, provided that the T-cells had identity in the I region of the H2 complex. K/D identity was neither necessary nor sufficient. It is concluded that transformation can be induced by E. granulosus in both T- and B-cells and that, at least in naïve T-cells, the stimulus can be an I region-restricted, macrophage-presented signal.

Animals↗
PubMed1985

Suppression of induced erythrocyte autoantibodies is dependent on Lyt 1 cells.

When normal mice are immunized with rat RBC, autoantibodies to mouse red cells and antigen-specific suppressor cells are generated. Suppressor cell activity is found in T-enriched populations and suppresses only the induction of autoantibody, not ongoing or secondary autoantibody responses. Using antibodies lytic for either B cells or distinct T-cell subpopulations, we are able to show that suppression is dependent on the presence of Lyt 1+ T cells.

Animals↗
PubMed1983

Heterogeneity of B-cells.

Two rat monoclonal antibodies, NIM-R2 and NIM-R3, were prepared that only recognize B-cells in murine secondary lymphoid tissues. Both showed differential reactivity in that they reacted most strongly with nonoverlapping populations of B-cells. They also reacted differentially with some cells of the primary lymphoid tissue, recognizing 90-95% of bone marrow cells, again in a nonoverlapping manner and with NIM-R2 accounting for twice as many cells as NIM-R3. The antibody NIM-R2, but not NIM-R3, also recognized thymocytes and red blood cells. The determinant recognized by NIM-R2 is of interest because it fluctuates at four defined stages of B-cell development: pre-B to immature B, activation of mature B, differentiation of memory cells, and differentiation of antibody-secreting cells. Particularly noteworthy was the differential reactivity of NIM-R2 with virgin and memory B-cells. Those cells that stained strongly with the antibody gave excellent primary responses, but were unable to transfer secondary responses, whereas weakly stained B-cells transferred memory, but could not generate primary antibody responses in vitro. Thus NIM-R2 recognized a cell-surface determinant that presumably decreases in density as primary B-cells differentiate into memory B-cells. A survey of sIg, I-A, Fc receptors, and major glycoproteins of B-cells from spleen, Peyer's patches, mesenteric lymph nodes, and peripheral lymph nodes failed to reveal any major differences between the cells from these different lymphoid organs.

Animals↗
PubMed1983

The expression of surface IgD on B cells responsive to thymus-independent and thymus-dependent antigens and its requirement for B-cell triggering.

Cells separated by the fluorescence activated cell sorter on the basis of their surface IgD (sIgD) phenotype have been examined for responsiveness to thymus-dependent and thymus-independent antigens. The ability of monoclonal anti-IgD alloantibodies to inhibit responses in vitro to the various classes of antigen has also been investigated. Evidence is presented indicating that both sIgD positive and sIgD negative cells can respond to all types of antigen tested. However, although the presence of sIgD was necessary for the response of sIgD positive cells to thymus-dependent antigens, the presence of this isotype was not obligatory for the response of the sIgD positive population to thymus independent antigens. The possible role of sIgD as the obligatory purveyor of a B-cell activation signal is discussed in the light of these findings.

Animals↗
PubMed1980

Lack of autoantigen-specific splenic suppressor cells in mice with an X-linked B-lymphocyte defect.

Male and female progeny of a cross between CBA/N female and BALB/c male mice were tested for their ability to generate autoantigen-specific suppressor cells as a result of stimulation with crossreacting rat RBC. Male mice, hemizygous for the X-linked defect, were unable to generate these antigen-specific suppressor cells, whereas their female littermates behaved like the normal (CBA/Ca x BALB/c)F1 mice.

Animals↗
PubMed1979

Deficient production of anti-red cell autoantibodies by mice with an X-linked B lymphocyte defect.

The production of anti-self red cell antibodies has been studied in mice bearing the CBA/N X-linked B lymphocyte defect and their phenotypically normal littermates. Defective mice produced anti-self red blood cell (RBC) antibodies at markedly reduced levels after multiple injections of rat RBC. They also failed to show significant numbers of plaque-forming cells against enzyme-treated isologous RBC. These findings are discussed in terms of the nature of the CBA/N defect and the acquisition of a complete specificity repertoire.

Animals↗
PubMed1978

Ontogeny of murine-B-lymphocytes. Avidity of antigen binding cells in neonatal and adult mice.

The heterogeneity of avidity of DNP-binding (rosetting) cells has been studied in mice of various ages, in an attempt to learn more about the development of antibody diversity. The results indicate that during the neonatal period murine B cells show a limited heterogeneity of avidity with no "high" avidity ABC being detectable. This implies that the full repertoire of anti-DNP antibodies is only gradually acquired during ontogeny. The results are interpreted as favouring the hypothesis that somatic events are important in the generation of antibody diversity.

Aging↗
PubMed1978

Differential tolerance of thymus-independent and thymus-dependent antibody responses.

The effect of pre-immunization with soluble haptenated serum proteins or haptenated carbohydrates on the subsequent responses to the hapten in thymus-dependent or thymus-independent form was investigated. In certain cases both thymus-dependent and -independent responses were suppressed whilst in others a differential suppression of thymus-independent responsiveness was observed. These results are discussed in terms of B-cell subpopulations and mechanisms of tolerance induction.

Animals↗
PubMed1975

Age-dependent changes in the relative affinity of anti-dinitrophenyl antibodies in mice.

The affinity of anti-DNP antibodies produced by mice of various ages has been studied at the cellular level by the plaque inhibition technique. The affinity of PFC produced shortly after a single injection of antigen was found to increase during the first 6 weeks of life. The responses of 1- and 2-week-old animals also showed apparently restricted heterogeneity. The difference in the affinity of anti-DNP--PFC between young and adult mice could not be attributed to different (serum) levels of antigen or to differences in the rate of maturation of affinity during the immune response. Cell transfer experiments suggested that the age-dependent increase was due to a change in the population of antibody-forming (B) cell precursors and not to a progressive improvement of T-cell function. This findings is interpreted as favouring somatic mutation theories of antibody diversity.

Age Factors↗