No abstract available.
Humans ; Killer Cells, Lymphokine-Activated* ; Killer Cells, Natural*

OBJECTIVESTo evaluate the effects of K562-dendritic cell (DC) and Raji-DC fusion vaccines on the cytotoxicity of cord blood (CB) derived cytokine-induced killer/natural killer (CIK/NK) cells.

METHODSDC and CIK/NK cells were derived from CB mononuclear cells. CB-DC were fused with inactivated K562 or Raji cells by PEG to form K562 or Raji-DC fusion vaccine. The CIK/NK cells stimulated by different co-culture antigens were three groups: K562-DC or Raji-DC fusion vaccine group, inactivated K562 or Raji plus DC group, and CB-DC alone group. The cytotoxicity of CIK/NK cells stimulated by different co-culture antigens was measured by MTT test.

RESULTSAll the antigens used for stimulation could enhance the cytotoxicity of CB-CIK/NK cells, with no specificity difference. At 20:1 effector-target ratio, the cytolytic activities of K562-DC and Raji-DC fusion vaccine groups against Raji cells were (75.44 +/- 4.19)% and (81.33 +/- 4.18)% respectively (P < 0.05); and that of inactivated K562 + DC and Raji + DC group against Raji cells were (73.12 +/- 4.22)% and (80.49 +/- 4.27)%, respectively (P < 0.01). There was no significant difference in the cytotoxicity to K562 cells between the two fusion vaccine groups (P > 0.05). The cytotoxicity of CB-CIK/NK cells immunized by Raji cells was higher than that by K562 cells. In CIK/NK cells co-stimulated by the same tumor antigen, there was no significant difference in the cytotoxicity between DC fusion vaccine group and inactivated cells plus DC group to different tumor cells.

CONCLUSIONSThe cytotoxicity of CB-CIK/NK cells to tumor cells was not specific. There was no significant difference in the cytotoxic activity of CB-CIK/NK cells between the DC fusion vaccine group and inactivated cells plus DC group.

Cancer Vaccines ; immunology ; pharmacology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Dendritic Cells ; immunology ; Fetal Blood ; cytology ; Humans ; K562 Cells ; Killer Cells, Lymphokine-Activated ; immunology ; Killer Cells, Natural ; immunology

No abstract available.
Carps* ; Killer Cells, Natural

No abstract available.
Killer Cells, Natural* ; Psoriasis*

No abstract available.
Killer Cells, Natural* ; Psoriasis*

Natural killer (NK) cells play a pivotal role in early surveillance against virus infection and cellular transformation, and are also implicated in the control of inflammatory response through their effector functions of direct lysis of target cells and cytokine secretion. NK cell activation toward target cell is determined by the net balance of signals transmitted from diverse activating and inhibitory receptors. A distinct feature of NK cell activation is that stimulation of resting NK cells with single activating receptor on its own cannot mount natural cytotoxicity. Instead, specific pairs of co-activation receptors are required to unleash NK cell activation via synergy-dependent mechanism. Because each co-activation receptor uses distinct signaling modules, NK cell synergy relies on the integration of such disparate signals. This explains why the study of the mechanism underlying NK cell synergy is important and necessary. Recent studies revealed that NK cell synergy depends on the integration of complementary signals converged at a critical checkpoint element but not on simple amplification of the individual signaling to overcome intrinsic activation threshold. This review focuses on the signaling events during NK cells activation and recent advances in the study of NK cell synergy.
Killer Cells, Natural ; Viruses

BACKGROUND: Murine IL-2-induced lymphokine-activated killers can be divided into two mutually exclusive subset:NK1.1'CD8 and NK1.1 CD8+. However, there is a strong evidence that NK cell may belong to T cell lineage. Recently novel lymphocyte subsets, present in the adult murine thymus, CD3+NK1.1'TCRap(TNK) cell is readily identifiable in fresh obtained murine adult CD4 CD8 thymocytes. MATERIAL AND METHOD: We sorted out CD4 and CD8 (double negative.' DN) cells and CD8+ cells from murine spleen and cultivated these cells with IL-2. And the surface B220, CD8, NK1. 1 and cytopasmic NK1.1 was analysed simultaneously to see whether these cells can be switched to the other subtype of cells. RESULT: Purified DN cells were switched to several subtype of cells'. CD8'B220+(LAK cells), NK1.1'B220+(LAK cells), CD8 B220, cytoplasmic NK1.1+B220 cells. Purified CD8 cells were switched to CD8+B220' LAK cells and cytoplasmic NK1.1+ CD8+ B220+ and cytoplasmic NK1.1' CD8 B220 cells. In addition, the CD8' cells originated from DN cells do not express the cytoplasmic NK1.1 in contrary to the sorted CD8 cells. CONCLUSION: Our results indicated that these will be useful models to investigating CD8 precursor potentials in populations of CD4 CD8 (doble negative) cells and relationship of NK1.1 These results also supports the hypothesis that T cells and NK cells have same ontogeny and CD8 effector functions are potentially diverse and could be exploited by various conditions that switch off host protected cytolytic response. These model offer a way to study the molecular regulation of CD8 gene expression.
Adult ; Cell Lineage ; Cytoplasm ; Gene Expression ; Humans ; Interleukin-2* ; Interleukins* ; Killer Cells, Lymphokine-Activated ; Killer Cells, Natural ; Lymphocyte Subsets ; Spleen ; T-Lymphocytes ; Thymocytes ; Thymus Gland

No abstract available.
Animals ; Killer Cells, Natural* ; Mice*

No abstract available.
Dermatitis, Atopic* ; Killer Cells, Natural*

No abstract available.
Hematologic Neoplasms* ; Killer Cells, Natural*