摘要:

AbstractKinetic analysis was used to define lytic events in peripheral blood mnonuclear cells (Pm) activated in lymphkine conditioned medium (LCM) and recanbinant interleukin-2 (rIL-2). This analysis provided quantitative information on the functional properties of these lymphkine-activated killer (LAK) cells against NK-resistant and NK-sensitive tumor cell lines. the maximum rate of target cell lysis (Vmax) and Km (target cell number resulting in 1/2 Vmax) were determined. IL-2 activated effector cells that bound to target cells also lysed them (i.e., non-lytic bystander lymphocytes did not influence the determination of kinetic parmters) in contrast to lysis mediated by unactivated NK cells. the extent of LAK cell binding to tmr target cells was dependent upon the tumor type. LAK cell frequency determinations were calculated where Km approximated the concentration of LAK cells that were capable of killing a particular target. LAK cells generated in rIL-2 were lytically more efficient than those activated in LCM, and T-depletion resulted in a LAK population with the highest maximum rate of lysis. the use of kinetic analysis to evaluate LAK cell frequencies and quantitate lytic events will be useful in determining the effects of drugs, biological response modifiers and disease states on LAK cell function.

ISSN:0892-3973    

DOI:10.3109/08923979109019697

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

AbstractExogenous PGE2 strongly inhibits the response of human lymphocyte cultures to SRBC. This effect is mediated through a T cell inhibition since non-T cells are not significantly affected. Indomethacin, which inhibits in this system lymphocyte endogenous PGE2 synthesis increases the in vitro immune response. the effect of indomethacin is overcame by exogenous PGE2. These data may be relevant for explaining the immunomodulatory role of PGE2 following antigen challenge.

ISSN:0892-3973    

DOI:10.3109/08923979109019698

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

AbstractRecombinant human granulocyte/macrophage colony-stimulating factor (GM-CSF) induced significant superoxide production in human neutrophils within 30 minutes after addition of stimulus and the response was complete within 2 hr. Other agents known to prime neutrophils, including LPS and tumor necrosis factor-a, lacked activity under the experimental conditions employed. Using a panel of pharmacologic inhibitors, we sought to compare GM-CSF-induced neutrophil superoxide to that produced by cells exposed to N-formyl methionyl-leucyl-phenylalanine (fMet-Leu-Phe) and phorbol 12–myristate 13–acetate (PMA). Each stimulant displayed a different profile. Rolipram, a peak IV phosphodiesterase inhibitor, specifically inhibited neutrophil activation by GM-CSF and fMet-Leu-Phe, while superoxide production stimulated by PMA was unaffected. Staurosporine, a protein kinase C (PK-C) inhibitor, suppressed superoxide production induced by all three neutrophil stimulants. Cytochalasin B totally inhibited superoxide induced by GM-CSF under conditions that promote the fMet-Leu-Phe-induced response. Cytochalasin B did not markedly affect PMA-induced superoxide. the results are consistent with the hypothesis that intact PK-C activity is essential for neutrophil superoxide production, but that differences exist in the initial pathways induced by these neutrophil activators. Superoxide secretion from GM-CSF-treated neutrophils appears to be a direct, delayed response that requires assembly of microfilaments during exposure to the cytokine.

ISSN:0892-3973    

DOI:10.3109/08923979109019699

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

摘要:

AbstractNFS60, a murine leukemia cell line, responds to both interleukin 3 and 6 by proliferating, apparently by different signal transduction pathways. Although stimulation by both cytokines increases the uptake of3H-arachidonic acid, the response to IL-6 was much faster. Furthermore, the effect of various arachidonic acid metabolites on the response to cytokine was different. PGE2 inhibited IL-6–induced proliferation and potentiated the response to IL-3. Additionally the G proteins which coupled the IL-3 and IL-6 receptor to the proliferative response are probably different, based on the ability of cholera toxin to inhibit the IL-3 but not the IL-6 response. These data are evidence of two pathways of signal transduction.

ISSN:0892-3973    

DOI:10.3109/08923979109019700

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor

ISSN:0892-3973    

DOI:10.3109/08923979109019701

出版商:Taylor&Francis    

年代:1991

数据来源: Taylor