Search

We investigate temperature-dependent carrier dynamics of InAs crystal by using reflection-type terahertz time-domain spectroscopy, particularly with a recently developed emitter–sample hybrid structure. We successfully obtain the optical conductivity in a terahertz frequency of bulk InAs whose dc conductivity is in the range of 100–150  Ω^−1 cm^−1. We find that both real and imaginary parts of the optical conductivity can be fit well with the simple Drude model, and the free-carrier density and the scattering rate obtained from the fit are in good agreement with corresponding values obtained by using other techniques, such as the Hall measurement and the dc-resistivity measurement. These results clearly demonstrate that the proposed technique of adopting the emitter–sample hybrid structure can be exploited to determine temperature-dependent optical constants in a reflection geometry and hence to investigate electrodynamics of bulk metallic systems.

Interleukin‐12 (IL‐12) may play a central role in the development and progression of rheumatoid arthritis by driving the immune response towards T helper 1 (Th1) type responses characterized by high IFN‐γ and low IL‐4 production. In this study we investigated the effect of auranofin (AF), an anti‐rheumatic gold compound, on IL‐12 production in mouse macrophages and dendritic cells, and studied whether AF‐mediated inhibition of IL‐12 production could regulate a cytokine profile of antigen (Ag)‐primed CD4+Th cells.Treatment with AF significantly inhibited IL‐12 production in lipopolysaccharide (LPS)‐stimulated macrophages and also in CD40L‐stimulated dendritic cells. AF‐pretreated macrophages reduced their ability to induce IFN‐γ and increased the ability to induce IL‐4 in Ag‐primed CD4+T cells. AF did not influence the cell surface expression of the class II MHC molecule and the costimulatory molecules CD80 and CD86.Addition of recombinant IL‐12 to cultures of AF‐pretreated macrophages and CD4+T cells restored IFN‐γ production in Ag‐primed CD4+T cells.The in vivoadministration of AF resulted in the inhibition of IL‐12 production by macrophages stimulated in vitrowith LPS or heat‐killed Listeria monocytogenes(HKL), leading to the inhibition of Th1 cytokine profile (decreased IFN‐γ and increased IL‐4 production) in Ag‐primed CD4+T cells.These findings may explain some known effects of AF including anti‐rheumatic effects and the inhibition of encephalitogenicity, and point to a possible therapeutic use of AF in the Th1‐mediated immune diseases such as autoimmune diseases.

Interleukin‐12 (IL‐12) plays a central role in the immune system by driving the immune response towards T helper 1 (Th1) type responses characterized by high IFN‐γ and low IL‐4 production. In this study we investigated whether retinoid‐mediated inhibition of interleukin‐12 production in mouse macrophages could regulate cytokine profile of antigen (Ag)‐primed CD4+Th cells.Pretreatment with retinoids (9‐cis‐RA, all‐trans‐RA, TTNPB) significantly inhibited IL‐12 production by mouse macrophages stimulated with lipopolysaccharide (LPS) or heated‐killed Listeria monocytogenes(HKL). Retinoid‐pretreated macrophages reduced their ability to induce IFN‐γ and increased the ability to induce IL‐4 in Ag‐primed CD4+T cells.Addition of recombinant IL‐12 to cultures of retinoid‐pretreated macrophages and CD4+T cells restored IFN‐γ production in CD4+T cells.The in vivoadministration of 9‐cis‐RA resulted in the inhibition of IL‐12 production by macrophages stimulated in vitrowith either LPS or HKL, leading to the inhibition of Th1 cytokine profile (decreased IFN‐γ and increased IL‐4 production) in CD4+T cells.These findings may explain some known effects of retinoids including the inhibition of encephalitogenicity, and point to a possible therapeutic use of retinoids in the Th1‐mediated immune diseases such as autoimmune diseases.

Lipopolysaccharide (LPS) increases the production of interleukin-12 (IL-12) from mouse macrophages via a kappaB site within the IL-12 p40 promoter. In this study, we found that retinoids inhibit this LPS-stimulated production of IL-12 in a dose-dependent manner. The NFkappaB components p50 and p65 bound retinoid X receptor (RXR) in a ligand-independent manner in vitro, and the interaction interfaces involved the p50 residues 1-245, the p65 residues 194-441, and the N-terminal A/B/C domains of RXR. Activation of macrophages by LPS resulted in markedly enhanced binding activities to the kappaB site, which significantly decreased upon addition of retinoids, as demonstrated by the electrophoretic mobility shift assays. In cotransfections of CV-1 and HeLa cells, RXR also inhibited the NFkappaB transactivation in a ligand-dependent manner, whereas a mutant RXR lacking the AF2 transactivation domain, which serves as ligand-dependent binding sites for transcription integrators SRC-1 and p300, was without any effect. In addition, coexpression of increasing amounts of SRC-1 or p300 relieved the retinoid-mediated inhibition of the NFkappaB transactivation. From these results, we propose that retinoid-mediated suppression of the IL-12 production from LPS-activated macrophages may involve both inhibition of the NFkappaB-DNA interactions and competitive recruitment of transcription integrators between NFkappaB and RXR.

Interleukin‐12 (IL‐12) plays a central role in the immune system by driving the immune response towards T helper 1 (Th1) type responses which are characterized by high IFN‐γ and low IL‐4 production. In this study we investigated the effects of curcumin, a natural product of plants obtained from Curcuma longa(turmeric), on IL‐12 production by mouse splenic macrophages and the subsequent ability of these cells to regulate cytokine production by CD4+T cells.Pretreatment with curcumin significantly inhibited IL‐12 production by macrophages stimulated with either lipopolysaccharide (LPS) or head‐killed Listeria monocytogenes(HKL).Curcumin‐pretreated macrophages reduced their ability to induce IFN‐γ and increased the ability to induce IL‐4 in Ag‐primed CD4+T cells. Addition of recombinant IL‐12 to cultures of curcumin‐pretreated macrophages and CD4+T cells restored IFN‐γ production in CD4+T cells.The in vivoadministration of curcumin resulted in the inhibition of IL‐12 production by macrophages stimulated in vitrowith either LPS or HKL, leading to the inhibition of Th1 cytokine profile (decreased IFN‐γ and increased IL‐4 production) in CD4+T cells.These findings suggest that curcumin may inhibit Th1 cytokine profile in CD4+T cells by suppressing IL‐12 production in macrophages, and points to a possible therapeutic use of curcumin in the Th1‐mediated immune diseases.