PubMed Health⌕ Search

Biomedical subjects

C S Henney

Publications and source records attributed to C S Henney.

At least 19 recordsLinked to original sources
PubMed1989

Interleukin 7: effects on early events in lymphopoiesis.

Recently, rapid progress has been made in defining and characterizing those growth factors associated with the major hemopoietic lineages. In contrast, the regulatory factors associated with the commitment and differentiation of precursor cells in the early events of lymphogenesis are much less clearly understood. In this review, Christopher Henney describes the isolation and characterization of one such factor-IL-7-and its effect on early B- and T-cell development.

Animals↗
PubMed1989

Early events in lymphopoiesis: the role of interleukins 1 and 7.

This article summarizes evidence that interleukins 1 and 7 play a critical role in the early stages of lymphopoiesis. IL-1 has been demonstrated to be identical to the growth factor previously termed haemopoietin-1 and appears to cause the growth of haemapoietic stem cells. Interleukin-7, originally described as a pre-B-cell growth factor, also has proliferative activity on T cells. It is proposed that IL-7 acts on lymphoid stem cells.

Animals↗
PubMed1989

Interleukin-1.

Explore the source record for details and available documents.

Amino Acid Sequence↗
PubMed1988

Hematopoietic activities of interleukin 1.

IL-1 is perhaps the most pleiomorphic of the cytokines. Only recently however has it been suspected that IL-1 has effects in stimulating hematopoiesis. Its principal effect in this regard seems to be stimulation of pluripotent stem cells, causing these cells to then respond to lineage-specific growth factors. Thus, although IL-1 does not function directly as a colony stimulating factor, it synergizes with G-CSF, GM-CSF, and IL-3. Indeed, biochemical and serological evidence suggests that IL-1 accounts totally for the biological activity previously termed hemopoietin-1 which has been shown to play a central role in the regulation of hematopoiesis.

Animals↗
PubMed1985

The treatment of induced immune deficiency with interleukin-2.

In vivo generation of alloreactive cytotoxic T lymphocytes (CTL) was found to be inhibited by treatment of mice with either cyclophosphamide or the glucocorticoid, hydrocortisone acetate. The effects of these immunosuppressive agents could be overcome, however, by the in vivo administration of IL-2 from both murine and human sources. Both human IL-2 derived by recombinant DNA techniques as well as the natural protein from mouse and man all reverse the unresponsive state. A single injection of IL-2 was sufficient to reverse the effect of cyclophosphamide treatment, while additional injections with as little as 8 micrograms of protein ablated the steroid-induced suppression. Furthermore, the responder cells generated in vivo following IL-2 therapy were shown to be antigen specific in terms of their lytic capacity. Thus, IL-2 therapy appears to restore the in vivo responsiveness of immunosuppressed recipients to allogeneic tumor cell challenge. These data demonstrate the importance of IL-2 as an immunoregulatory molecule in vivo and suggest its future use as a potent therapeutic.

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↗