Anisotropic properties of pipe-GaN distributed Bragg reflectors.

We report here a simple and robust process to convert periodic Si-doped GaN/undoped-GaN epitaxial layers into a porous-GaN/u-GaN distributed Bragg reflector (DBR) structure and demonstrate its material properties in a high-reflectance epitaxial reflector. Directional pipe-GaN layers with anisotropic optical properties were formed from n-GaN : Si layers in a stacked structure through a lateral and doping-selective electrochemical etching process. Central wavelengths of the polarized reflectance spectra were measured to be 473 nm and 457 nm for the pipe-GaN reflector when the direction of the linear polarizer was along and perpendicular to the pipe-GaN structure.

TGF-β regulated leukemia cell susceptibility against NK targeting through the down-regulation of the CD48 expression.

Transforming growth factor-β (TGF-β) is known to function as a dual role regulatory cytokine for being either a suppresser or promoter during tumor initiation and progression. In solid tumors, TGF-β secreted from tumor microenvironment acts as a suppresser against host immunity, like natural killer (NK) cells, to favor tumor evasion. However, besides solid tumors, the underlying mechanism of how TGF-β regulates leukemogenesis, tumor progression, immunoediting, and NK function is still not clear in detail.

A Developed NK-92MI Cell Line with Siglec-7 Phenotype Exhibits High and Sustainable Cytotoxicity against Leukemia Cells.

Altered sialic acid processing that leads to upregulation of cell surface sialylation is recognized as a key change in malignant tissue glycosylation. This cancer-associated hypersialylation directly impacts the signaling interactions between tumor cells and their surrounding microenvironment, especially the interactions mediated by immune cell surface sialic acid-binding immunoglobulin-like lectins (Siglecs) to relay inhibitory signals for cytotoxicity. First, we obtained a Siglec-7 NK-92MI cell line, NK-92MI-S7N, by separating a group of Siglec-7 cell population from an eight-month-long-term NK-92MI in vitro culture by fluorescence-activated cell sorting (FACS).

Branched I antigens on leukemia cells enhanced sensitivity against natural killer-cell cytotoxicity through affecting the target-effector interaction.

Background: The aberrant glycosylation on proteins and lipids has been implicated in malignant transformations for promoting the tumorigenesis, metastasis, and evasion from the host immunity. The I-branching β-1,6-N-acetylglucosaminyltransferase, converting the straight i to branched I histo-blood group antigens, reportedly could influence the migration, invasion, and metastasis of solid tumors.

Study Design And Methods: We first chose the highly cytotoxic natural killer (NK)-92MI cells as effector against leukemia for this cell line has been used in several clinical trials.

The SHP2-ERK2 signaling pathway regulates branched I antigen formation by controlling the binding of CCAAT/enhancer binding protein α to the IGnTC promoter region during erythroid differentiation.

Background: Phosphorylation status of the transcription factor CCAAT/enhancer binding protein α (C/EBPα) has been demonstrated in a human hematopoietic cell model to regulate the formation of branched I antigen by affecting its binding affinity to the promoter region of the IGnTC gene during erythroid and granulocytic differentiation.

Study Design And Methods: The K-562 cell line was induced to differentiate into red blood cells (RBCs) or granulocytes by sodium butyrate or retinoic acid, respectively, to study the involvement of three MAP kinase pathways in I antigen synthesis. The regulatory effects of the extracellular signal-regulated kinase (ERK)2-Src homology region 2 domain-containing phosphatase 2 (SHP2) pathway on phosphorylation status and binding affinities of C/EBPα as well as the subsequent activation of IGnTC and synthesis of surface I formation were studied in wild-type K-562 cells and in mutant cells that overexpress ERK2 and SHP2.