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C S Henney

Publications and source records attributed to C S Henney.

At least 55 records · Page 3Linked to original sources
PubMed1980

Identification of ganglio-N-tetraosylceramide as a new cell surface marker for murine natural killer (NK) cells.

The BCG-induced NK cell activity of murine peritoneal exudate cells was abolished by preincubation of effector cells with anti-ganglio-N-tetraosylceramide (anti-asialo GM1) and C but not with other anti-glycolipid antibodies, anti-ganglioside GM1, anti-globoside, and anti-ganglio-N-triosylceramide (anti-asialo GM2). In contrast, the cytotoxic activity of alloimmune T cells was not affected by treatment with anti-asialo GM1 antisera. These findings suggest that asialo GM1 display may be characteristic of NK cell populations and aid in the isolation of this population of cytotoxic cells.

Animals↗
PubMed1979

The generation and specificity of cytotoxic T cells raised against syngeneic tumor cells bearing AKR/Gross murine leukemia virus antigens.

Efforts were made to generate C57BL/6 cytotoxic effector cells to a syngeneic leukemia (E{male}G2) bearing AKR/Gross virus antigens. As we were unable to induce significant cytotoxic activity by immunization with up to 10(8) irradiated E{male}G2 cells, even when cells from such primed animals were subsequently restimulated with E{male}G2 cells in vitro, C57BL/6 mice were immunized with an aliogeneic, virus-producing AKR leukemic cell line (AKR SL3). Peritoneal exudate cells and, to a lesser degree, spleen cells from these mice showed significant lytic activity toward the immunizing allogeneic tumor but not toward E{male}G2. When spleen cells were harvested from animals {approximately equal to}10 d after injection of AKR SL3 and rechallenged in vitro with either E{male}G2 or AKR.H-2(b) SL1, another tumor that displays AKR/Gross virus antigens, then a vigorous cytotoxic response against E{male}G2 and AKR. H-2(b) SL1 was obtained. Effector cells generated by AKR SL3 priming followed by in vitro stimulation with E{male}G2 or AKR.H-2(b) SL1 lysed only cells of H-2(b) haplotype which were strongly positive for the display of serologically detectable AKR/Gross virus antigens. Thus, AKR SL3 cells were not lysed nor were EL4 cells (H-2(b); but only weakly positive for gp70). Cells not bearing the MuLV antigens tested for, such as P815 mastocytoma cells and spleen cell "blasts" from C57BL/6 and CBA (H-2(k)) mice, were also insusceptible to attack. The cytotoxic effector cells induced bore Thy 1.2 alloantigen and were of the Lyt 1+2+ phenotype. Collectively, these findings are consistent with the conclusion that the cytotoxic T cells raised against E{male}G2 are directed against AKR/Gross virus-associated antigens and are H-2 restricted. It will be of interest to determine the relevance of such effector cells to the known resistance of the C57BL/6 mouse to AKR/Gross virus-induced leukemia.

AKR murine leukemia virus↗
PubMed1979

The differentiation of cytotoxic T cells in vitro. I. Amplifying factor(s) in the primary response is Lyt 1 + cell dependent.

Within 15 hr of establishment of a murine mixed lymphocyte culture, a soluble mediator was produced that was capable of augmenting primary cytotoxic responses to alloantigen. The factor did not induce responsiveness in the absence of antigen, since the amplified response seen in its presence was specific for the stimulating alloantigen. The factor did not therefore appear to function by polyclonal activation of cytotoxic precursor cells. Production of the amplifying factor(s) was induced by unfractionated spleen cells, but not by cells subjected to UV irradiation or to sonication, making it likely that this deficiency is the basis of the well-documented failure of these stimulator cells to induce primary cytotoxic responses. The amplifying effects of the factor were distinctive from, but synergistic with, those of 2-mercaptoethanol. Production of the amplifying mediator did not require cell division but was dependent upon the presence of Lyt 1 + cells. On the other hand, Lyt 2 + cells were not needed for mediator production, but served as target cell population on which the factor exerted its action. These findings are compatible with the hypothesis that direct T-T cell collaboration can amplify the differentiation of cytotoxic cells.

Animals↗
PubMed1978

BCG-induced suppressor cells. I. Demonstration of a macrophage-like suppressor cell that inhibits cytotoxic T cell generation in vitro.

Spleen cells obtained from mice 5 to 40 days after infection with viable BCG organisms (BCG-spleens) were found to be unresponsive in vitro to both mitogenic and alloantigenic stimuli. Moreover, suppressor cells could be demonstrated in the spleens from these infected animals. When spleen cells from BCG-infected mice were added to either syngeneic or allogeneic normal spleen cells, the mixtures neither proliferated nor developed cytotoxic activity when cultured with alloantigen or with concanavalin A (Con A). The development of unresponsiveness post-infection paralleled the onset of suppressive activity. Spleen cells obtained from mice given heat-killed BCG were neither suppressive nor unresponsive. The suppressive activity of BCG-spleen cells was associated with an adherent, phagocytic cell that lacked membrane-associated Thy-1 antigen. Removal of this cell by passage through nylon wool columns resulted in a cell population that was no longer capable of suppression and that responded normally to alloantigen and to Con A. It would thus appear that BCG infection results in the development of a "suppressor" macrophage-like cell population within the spleen. The role of this cell type in regulation of the immune response in BCG-infected animals is as yet undefined.

Animals↗
PubMed1978

The use of cytochalasins to probe the immunobiolgoy of lymphocytes.

No attempt will be made to summarize in any formal way the "pot-pourri" of experiments we have considered in this chapter. It may occur to some that immunologists as a group have been somewhat removed from the advances made in cellular biology during the last decade. Specifically, they may appear to lack an appreciation of the many ways in which durgs like the cytochalasins can affect cell function. Perhaps because of this naivety however, the immunologists have used the cytochalasins to probe systems so complex that they would never have been comtemplated by more conservative investigaors. In doing so they have revealed insight into many systems that will hopefully be of broad biolgical interest. To date the insights have been mostly of a rather superficial nature and clearly demand more thorough investigation. If they are to be done, such studies will have to be performed by non-immunologists bringing new tools and new perspectives to bear on the immunologists' problems.

Animals↗