Cross-Linked Aptamer-Lipid Micelles for Excellent Stability and Specificity in Target-Cell Recognition

2018 ◽  
Vol 130 (36) ◽  
pp. 11763-11767 ◽  
Author(s):  
Xiaowei Li ◽  
C. Adrian Figg ◽  
Ruowen Wang ◽  
Ying Jiang ◽  
Yifan Lyu ◽  
...  
Keyword(s):  
Target Cell ◽  
Cell Recognition ◽  
Lipid Micelles ◽  
Excellent Stability

scholarly journals Cross‐Linked Aptamer–Lipid Micelles for Excellent Stability and Specificity in Target‐Cell Recognition

2018 ◽  
Vol 57 (36) ◽  
pp. 11589-11593 ◽  
Author(s):  
Xiaowei Li ◽  
C. Adrian Figg ◽  
Ruowen Wang ◽  
Ying Jiang ◽  
Yifan Lyu ◽  
...  
Keyword(s):  
Target Cell ◽  
Cell Recognition ◽  
Lipid Micelles ◽  
Excellent Stability

scholarly journals Recognition of virus-infected cells by natural killer cell clones is controlled by polymorphic target cell elements.

1993 ◽  
Vol 178 (3) ◽  
pp. 961-969 ◽  
Author(s):  
M S Malnati ◽  
P Lusso ◽  
E Ciccone ◽  
A Moretta ◽  
L Moretta ◽  
...  
Keyword(s):  
T Cells ◽  
Nk Cells ◽  
Natural Killer ◽  
Target Cell ◽  
Nk Cell ◽  
Class I ◽  
Target Cells ◽  
Cell Recognition ◽  
Infected Cells ◽  
Nk Cell Recognition

Natural killer (NK) cells provide a first line of defense against viral infections. The mechanisms by which NK cells recognize and eliminate infected cells are still largely unknown. To test whether target cell elements contribute to NK cell recognition of virus-infected cells, human NK cells were cloned from two unrelated donors and assayed for their ability to kill normal autologous or allogeneic cells before and after infection by human herpesvirus 6 (HHV-6), a T-lymphotropic herpesvirus. Of 132 NK clones isolated from donor 1, all displayed strong cytolytic activity against the NK-sensitive cell line K562, none killed uninfected autologous T cells, and 65 (49%) killed autologous T cells infected with HHV-6. A panel of representative NK clones from donors 1 and 2 was tested on targets obtained from four donors. A wide heterogeneity was observed in the specificity of lysis of infected target cells among the NK clones. Some clones killed none, some killed only one, and others killed more than one of the different HHV-6-infected target cells. Killing of infected targets was not due to complete absence of class I molecules because class I surface levels were only partially affected by HHV-6 infection. Thus, target cell recognition is not controlled by the effector NK cell alone, but also by polymorphic elements on the target cell that restrict NK cell recognition. Furthermore, NK clones from different donors display a variable range of specificities in their recognition of infected target cells.

Mechanism of target cell recognition by CD3− LGL

1992 ◽  
Vol 142 (1) ◽  
pp. 28-39 ◽  
Author(s):  
Tamar Bino ◽  
Joyce L. Frey ◽  
John R. Ortaldo
Keyword(s):  
Target Cell ◽  
Cell Recognition

scholarly journals Rapid biogenesis and sensitization of secretory lysosomes in NK cells mediated by target-cell recognition

2004 ◽  
Vol 102 (1) ◽  
pp. 123-127 ◽  
Author(s):  
D. Liu ◽  
L. Xu ◽  
F. Yang ◽  
D. Li ◽  
F. Gong ◽  
...  
Keyword(s):  
Nk Cells ◽  
Target Cell ◽  
Cell Recognition ◽  
Secretory Lysosomes

scholarly journals Regulation of human NK-cell cytokine and chemokine production by target cell recognition

Blood ◽  
2010 ◽  
Vol 115 (11) ◽  
pp. 2167-2176 ◽  
Author(s):  
Cyril Fauriat ◽  
Eric O. Long ◽  
Hans-Gustaf Ljunggren ◽  
Yenan T. Bryceson
Keyword(s):  
Nk Cells ◽  
Target Cell ◽  
Cell Activation ◽  
Nk Cell ◽  
Cell Recognition ◽  
Chemokine Production ◽  
Relative Contribution ◽  
Cytokines And Chemokines ◽  
Tnf Α ◽  
Ifn Γ

AbstractNatural killer (NK)–cell recognition of infected or neoplastic cells can induce cytotoxicity and cytokine secretion. So far, it has been difficult to assess the relative contribution of multiple NK-cell activation receptors to cytokine and chemokine production upon target cell recognition. Using Drosophila cells expressing ligands for the NK-cell receptors LFA-1, NKG2D, DNAM-1, 2B4, and CD16, we studied the minimal requirements for secretion by freshly isolated, human NK cells. Target cell stimulation induced secretion of predominately proinflammatory cytokines and chemokines. Release of chemokines MIP-1α, MIP-1β, and RANTES was induced within 1 hour of stimulation, whereas release of TNF-α and IFN-γ occurred later. Engagement of CD16, 2B4, or NKG2D sufficed for chemokine release, whereas induction of TNF-α and IFN-γ required engagement of additional receptors. Remarkably, our results revealed that, upon target cell recognition, CD56dim NK cells were more prominent cytokine and chemokine producers than CD56bright NK cells. The present data demonstrate how specific target cell ligands dictate qualitative and temporal aspects of NK-cell cytokine and chemokine responses. Conceptually, the results point to CD56dim NK cells as an important source of cytokines and chemokines upon recognition of aberrant cells, producing graded responses depending on the multiplicity of activating receptors engaged.

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