H. L. Park

A positive feedback loop of IL-21 signaling provoked by homeostatic CD4+CD25- T cell expansion is essential for the development of arthritis in autoimmune K/BxN mice.

Rheumatoid arthritis is a joint-specific autoimmune inflammatory disease of unknown etiology. The K/BxN mouse is a model of rheumatoid arthritis that is thought to be mainly due to autoantibody-mediated inflammatory responses. We showed previously that homeostatic proliferation of autoreactive CD4+ T cells is required for disease initiation in the K/BxN mice. In this study, we show that the homeostatically proliferating CD4+CD25− T cells produce IL-21. We generated IL-21R-deficient (IL-21R−/−) K/BxN mice and found that these mice were completely refractory to the development of spontaneous arthritis. They contained fewer CD4+ T cells with a reduced proportion of homeostatically proliferating cells, fewer follicular Th cells, and, surprisingly, more Th17 cells than their control counterparts. They also failed to develop IgG1+ memory B cells and autoantigen-specific IgG1 Ab-secreting cells. IL-21 induced expression of receptor activator of NF-κB ligand (RANKL) a regulator of osteoclastogenesis, and few RANKL-expressing infiltrates were found in the synovia of IL-21R−/− K/BxN mice. Thus, our results demonstrate that IL-21 forms a positive feedback autocrine loop involving homeostatically activated CD4+ cells and that it plays an essential role in the development of autoimmune arthritis by mechanisms dependent on follicular Th cell development, autoreactive B cell maturation, and RANKL induction but independent of Th17 cell function. Consistent with this, in vivo administration of soluble the IL-21R-Fc fusion protein delayed the onset and progression of arthritis. Our findings suggest that effective targeting of IL-21-mediated processes may be useful in treating autoimmune arthritis.

Molecular Mechanism of the Activation-Induced Cell Death Inhibition Mediated by a p70 Inhibitory Killer Cell Ig-Like Receptor in Jurkat T Cells

In this study we investigated the molecular mechanism of the activation-induced cell death (AICD) inhibition mediated by a p70 inhibitory killer cell Ig-like receptor (KIR3DL1, also called NKB1) in Jurkat T cells. Using stable Jurkat transfectants that express KIR or CD8-KIR fusion proteins we have shown for the first time that KIR inhibits, in a ligation-independent manner, the AICD induced by PHA, PMA/ionomycin, or anti-CD3 Ab. The AICD inhibition mediated by KIR appears to result from the blockade of Fas ligand induction upon activation of the Jurkat transfectants. Moreover, the membrane-proximal 20 aa of the KIR cytoplasmic tail were determined to play a crucial role in this process. Since the membrane-proximal portion of the KIR cytoplasmic tail contains a putative protein kinase C (PKC) substrate site, we investigated the molecular interaction between KIR and PKC. Immunoprecipitation analysis demonstrated that KIR constitutively bound both to PKCα, a conventional Ca2+-dependent PKC, and to PKCθ, a novel Ca2+-independent PKC. Furthermore, an in vitro kinase assay revealed that PKC activation was blocked after PHA stimulation in Jurkat transfectants expressing KIR. These observations were supported by the finding that a recombinant KIR cytoplasmic tail also appeared to inhibit PKCα activation in vitro. Taken together these data strongly suggest that KIR inhibits the AICD of T cells by blocking Fas ligand induction upon stimulation, in a process that seems to be accomplished by PKC recruitment to the membrane-proximal PKC binding site and subsequent inhibition of PKC activation against the activating stimuli.

Phase studies of SrOAl2O3 by emission signatures of Eu2+ and Eu3+

Phase transformation sequences of SrOue5f8Al2O3 have been investigated at 1000 and 1250 °C through XRD technique along with emission signatures of Eu2+ and Eu3+. Two phases, i.e., [Sr3Al2O6] and [SrAl2O4], have been observed at 1000 °C as stable phases. These phases were found to be transformed into [SrAl2O4] at 1250 °C.

Tunable Color Emission in a Zn1−xCdxGa2O4 Phosphor and Solid Solubility of CdGa2O4 in ZnGa2O4

Abstract Tunable color emission was achieved through forming solid solution between ZnGa 2 O 4 and CdGa 2 O 4 , i.e., Zn 1−x Cd x Ga 2 O 4 . The solid solubility limit of CdGa 2 O 4 in ZnGa 2 O 4 was found to be 0.6 mole fraction. Thus, solid solution can exist in 0 ≤ x ≤ 0.6 compositions in the Zn 1−x Cd x Ga 2 O 4 . Emission color was tunable between 352 and 520 nm in Zn 1−x Cd x Ga 2 O 4 (0 ≤ x ≤ 0.6). Our approach has demonstrated an innovative way of tuning color through the formation of solid solution between CdGa 2 O 4 and ZnGa 2 O 4

Growth of CdTe epitaxial films on p‐InSb(111) by temperature gradient vapor transport deposition

The growth of high quality CdTe epitaxial films on p‐InSb(111) by a simple method of temperature gradient vapor transport deposition was carried out to investigate the possibility of the existence of a two‐dimensional electron gas with high mobility at CdTe/InSb heterointerfaces. From the x‐ray diffraction analysis, the grown layer was found to be a CdTe epitaxial film. Photoluminescence measurements at 15 K showed that a CdTe film grown on InSb(111) in the temperature range between 180 and 280u2009°C appeared to have an optimum crystal perfection at a substrate temperature of about 245u2009°C. These results also indicated that the CdTe films grown above 245u2009°C contained a significant problem due to interdiffusion from the InSb substrates during the growth.

Characteristics of the killing mechanism of human natural killer cells against hepatocellular carcinoma cell lines HepG2 and Hep3B

PurposeUnlike normal hepatocytes, most hepatocellular carcinomas (HCCs) are quite resistant to death receptor-mediated apoptosis when the cell surface death receptor is cross linked with either agonistic antibodies or soluble death ligand proteins in vitro. The resistance might play an essential role in the escape from the host immune surveillance; however, it has not been directly demonstrated that HCCs are actually resistant to natural killer (NK) cell-mediated death. Therefore, this study investigated the molecular mechanism of NK cell-mediated cytotoxicity against the HCCs, HepG2, and Hep3B, using two distinct cytotoxic assays: a 4-h 51Cr-release assay and a 2-h [3H] thymidine release assay which selectively measures the extent of necrotic and apoptotic target cell death, respectively.MethodsMost of the target cells exhibited marked morphologic changes when they were co-incubated with the NK cells, and the NK cytotoxicity against these HCCs was comparable to that against K562, a NK-sensitive leukemia cell line, when the cytotoxicity was assessed by a 4-h 51Cr release assay.ResultsThe NK cells also induced significant apoptotic cell death in the Hep3B targets, but not in the HepG2 targets, when the cytotoxicity was assessed by a 2-h [3H]-thymidine release assay. In agreement with these results, procaspase-3 was activated in the Hep3B targets, but not in the HepG2 targets. Interestingly, mildly fixed NK cells had no detectable activity in the 4-h 51Cr release assay against both HepG2 and Hep3B targets, while they were similarly effective as the untreated NK cells in the 2-h [3H]-thymidine release assay, suggesting that the level of apoptotic cell death of the Hep3B targets is granule independent and might be primarily mediated by the death ligands of the NK cells.ConclusionThis study found that a tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor interaction is involved in the NK cell-mediated apoptotic death of the Hep3B targets, but a Fas/Fas ligand (FasL) interaction is not.

Stability of sulfur-treated InP surface studied by photoluminescence and x-ray photoelectron spectroscopy

The degradation behavior of the sulfur-treated InP surface at relatively low temperature has been investigated with x-ray photoelectron and photoluminescence (PL) spectroscopy. The results showed that the treated surfaces were oxidized to In2O3, InPO3, and InPO4 at 250u2009°C and in a vacuum of 10−3 Torr for 20 min. As the holding time for S-treated InP under a vacuum of 10−3 Torr increased, the PL peak caused by the band edge transition decreased without the formation of oxides. It was therefore suggested that the decrease of the PL intensity for S-treated InP is only related to the generation of phosphorous vacancies at the surface, not to oxide formation. The usefulness of a thin S overlayer on III–V semiconductors was also discussed.

Observation of the Burstein—Moss shift in heavily Te-doped In0.5Ga0.5P layers grown by liquid phase epitaxy

Abstract The Burstein—Moss shift was observed for the first time in heavily Te-doped In0.5Ga0.5P epilayers grown by liquid phase epitaxy. The photoluminescence transition energy was calculated using the carrier concentration dependent Fermi energy and the obtained value showed good agreement with the experimentally observed value. The origin of the observed photoluminescence transition can be portrayed as the k non-conserving transitions between the electrons in the higher energy level of the conduction band and the localized holes in the deeper tail state which is located on the top of the valence band. The carrier concentrations lie in the range from 1.5 × 1018 to 4.9 × 1018 cm−3.

Interdiffusion problems at CdTe/InSb heterointerfaces grown by temperature gradient vapor transport deposition

CdTe epitaxial films were grown by a simple method of temperature gradient vapor transport deposition on p‐InSb (111) orientation substrates in the growth temperature range between 200 and 280u2009°C. Raman spectroscopy showed the optical phonon modes of the CdTe thin films and the formation of an indium telluride interfacial layer in the CdTe/InSb heterostructures. The stoichiometry of the CdTe/InSb heterostructures was observed by the Auger electron spectroscopy, and Auger depth profiles also demonstrated that the CdTe/InSb heterointerface was not abrupt. The results indicated that the films grown at about 265u2009°C posed a significant problem due to interdiffusion from the InSb substrates during the growth.

Indirect energy transfer of Ce3+ → Eu2+ in CaAl12O19 phosphor

Photoluminescence characteristics and the energy transfer between Ce3+ and Eu2+ in CaAl12O19 host lattice have been investigated. A series of concentrations of Ce3+ ion with a fixed Eu2+ concentration in doubly doped CaAl12O19 : Ce3+Eu2+ have been studied. The indirect energy transfer has been observed between Ce3+ and Eu2+ through the Ce3+ue5f8OMe complex in CaAl12O19 host lattice. The two nonradiative relaxation processes from the excited levels of Ce3+ue5f8OMe complex; one, to the lower emitting level of Ce3+ue5f8OMe complex themselves and the other, to the Eu2+ site are competing processes.