1,720,994 research outputs found
Ligand binding to Fc gamma R induces c-myc-dependent apoptosis in IL-2-stimulated NK cells.
No full textThe role of signals transduced via Fc gamma RIIIA in the modulation of the proliferative potential of NK cells has been investigated. Fc gamma R stimulation does not induce NK cell proliferation, and inhibits that induced by IL-2, but not by IL-12, as measured by [3H]TdR incorporation, without affecting entrance or progression through cell cycle. The inhibitory effect depends, at least in part, on induced apoptosis of the cells, detected by both light and electron microscopy examination. Fc gamma R stimulation induces apoptosis only in NK cells that have been previously activated by IL-2: this occurs within 3 h from receptor stimulation and is independent from de novo receptor-induced RNA or protein synthesis, but requires receptor-induced activation of protein tyrosine kinases and extracellular Ca2+ influx. IL-2 induces accumulation of c-myc mRNA in NK cells, and treatment of the cells with c-myc antisense oligodeoxyribonucleotides during the IL-2 stimulation phase inhibits the susceptibility to Fc gamma RIIIA-induced cell death, indicating that the induction of sustained levels of this proto-oncogene is necessary for the phenomenon. Thus, a two-step model is suggested for the Fc gamma R-induced apoptosis in IL-2 activated NK cells: the first step involves induced expression of c-myc, and possibly other permissive factors, upon IL-2 prestimulation; the second depends directly on the stimulation of the receptor, independently of additional gene induction. The evidence presented here suggests a mechanism of control of NK cell expansion at the latest stages of Ab-dependent immune responses
Tumor necrosis factor and immune interferon synergistically induce cytochrome b-245 heavy-chain gene expression and nicotinamide-adenine dinucleotide phosphate hydrogenase oxidase in human leukemic myeloid cells.
No full textA novel surface marker (B203.13) of human haemopoietic progenitors,preferentially expressed along the B and myeloid lineages
No full textWe used a monoclonal antibody (mAb) (B203.13, IgM) generated from a mouse
immunized with the human B/myeloid bi-phenotypic B1b cell line, to analyse
haemopoietic cells. The antigen recognized by this mAb is expressed on most adult
and umbilical cord blood CD21+ B cells, at minimal density on mature monocytes,
and is undetectable on granulocytes, T, natural killer (NK) cells, and
erythrocytes. Within umbilical cord blood and adult bone marrow haemopoietic
progenitor cells, the B203.13 mAb recognized a surface marker, present on
progenitor cells of several haemopoietic lineages, that was transiently expressed
on early erythroid and T/NK progenitors, and was preferentially maintained on
cells of the B and myeloid lineages. Within the CD34+ cells, B203.13 was
expressed on early committed myeloid (CD33+) and erythroid (CD71dim) progenitor
cells, as confirmed in colony formation assays. The mAb also reacted with cells
of B and myeloid chronic leukaemias and cell lines. These data define B203.13 mAb
as a novel reagent useful for the characterization of haemopoietic progenitors
and leukaemias
EXPRESSION OF TYPE 1 (IFN-GAMMA) AND TYPE 2 (IL-13, IL-5) CYTOKINES AT DISTINCT STAGES OF NK CELL DIFFERENTIATION FROM PROGENITOR CELLS
No full textNATURAL KILLER (NK) CELL-MEDIATED CYTOTOXICITY: DIFFERENTIAL USE OF TRAIL AND FAS LIGAND BY IMMATURE AND MATURE PRIMARY HUMAN NK CELLS
No full textDEFINITION OF A NATURAL KILLER NKR-P1A+/CD56-/CD16- FUNCTIONALLY IMMATURE HUMAN NK CELL SUBSET THAT DIFFERENTIATES IN VITRO IN PRESENCE OF INTERLEUKIN 12
No full textFc gamma R(CD16) interaction with ligand induces Ca2+ mobilization and phosphoinositide turnover in human natural killer cells. Role of Ca2+ in Fc gamma R(CD16)-induced transcription and expression of lymphokine genes.
No full textExposure of platelet fibrinogen-binding sites by collagen, arachidonic acid, and ADP: inhibition by a monoclonal antibody to the glycoprotein IIb-IIIa complex.
No full textStimulation and proliferation of CD4+ peripheral blood T lymphocytes induced by an anti-CD4 monoclonal antibody.
No full textThere is experimental evidence that the CD4 molecule participates in the antigen-driven activation of T cells expressing this surface glycoprotein. Whether CD4, a member of the immunoglobulin supergene family, acts as a ligand-binding molecule and/or is directly involved in the activation pathway has yet to be established. In this study, we show that human CD4+ lymphocytes can be activated by exposure to the anti-CD4 monoclonal antibody (mAb) B66. Normal peripheral blood CD4+ cells were induced to proliferate and to synthesize interleukin 2 (IL 2) by the antibody. The specificity of the antibody stimulatory activity was tested by using IL 2-producing clones bearing either CD4 or CD8 on their surface. IL 2 production was induced by mAb B66 in CD4+, but not CD8+, clones, whereas both types of clones responded to stimulation by the anti-CD3 mAb Leu-4. Despite its unique stimulatory activity, mAb B66 shared with other anti-CD4 antibodies the ability to inhibit the specific cytolytic activity of CD4+ effector cells. These results clearly indicate that cross-linking of surface CD4 molecules with appropriate antibodies can fully activate CD4+ lymphocytes. Whether the natural ligand for CD4 can trigger this activation pathway remains to be defined
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