Context. A complex environment exists in the inner few astronomical units of planet-forming disks. High-angular-resolution observations play a key role in our understanding of the disk structure... Show moreContext. A complex environment exists in the inner few astronomical units of planet-forming disks. High-angular-resolution observations play a key role in our understanding of the disk structure and the dynamical processes at work.Aims: In this study we aim to characterize the mid-infrared brightness distribution of the inner disk of the young intermediate-mass star HD 163296 from early VLTI/MATISSE observations taken in the L- and N-bands. We put special emphasis on the detection of potential disk asymmetries.Methods: We use simple geometric models to fit the interferometric visibilities and closure phases. Our models include a smoothed ring, a flat disk with an inner cavity, and a 2D Gaussian. The models can account for disk inclination and for azimuthal asymmetries as well. We also perform numerical hydrodynamical simulations of the inner edge of the disk.Results: Our modeling reveals a significant brightness asymmetry in the L-band disk emission. The brightness maximum of the asymmetry is located at the NW part of the disk image, nearly at the position angle of the semimajor axis. The surface brightness ratio in the azimuthal variation is 3.5 ± 0.2. Comparing our result on the location of the asymmetry with other interferometric measurements, we confirm that the morphology of the r < 0.3 au disk region is time-variable. We propose that this asymmetric structure, located in or near the inner rim of the dusty disk, orbits the star. To find the physical origin of the asymmetry, we tested a hypothesis where a vortex is created by Rossby wave instability, and we find that a unique large-scale vortex may be compatible with our data. The half-light radius of the L-band-emitting region is 0.33 ±0.01 au, the inclination is 52°(-7°/+5°), and the position angle is 143° ± 3°. Our models predict that a non-negligible fraction of the L-band disk emission originates inside the dust sublimation radius for μm-sized grains. Refractory grains or large (≳10 μm-sized) grains could be the origin of this emission. N-band observations may also support a lack of small silicate grains in the innermost disk (r ≲ 0.6 au), in agreement with our findings from L-band data. Show less
Abuter, R.; Accardo, M.; Adler, T.; Amorim, A.; Anugu, N.; Ávila, G.; ... ; Zins, G. 2019
Fas ligand (FasL) not only induces apoptosis in Fas receptor-bearing target cells, it is also able to transmit signals into the FasL-expressing cell via its intracellular domain (ICD). Recently, we... Show moreFas ligand (FasL) not only induces apoptosis in Fas receptor-bearing target cells, it is also able to transmit signals into the FasL-expressing cell via its intracellular domain (ICD). Recently, we described a Notch-like proteolytic processing of FasL that leads to the release of the FasL ICD into the cytoplasm and subsequent translocation into the nucleus where it may influence gene transcription. To study the molecular mechanism underlying such reverse FasL signaling in detail and to analyze its physiological importance in vivo, we established a knockout/knockin mouse model, in which wild-type FasL was replaced with a deletion mutant lacking the ICD. Our results demonstrate that FasL ICD signaling impairs activation-induced proliferation in B and T cells by diminishing phosphorylation of phospholipase C gamma, protein kinase C, and extracellular signal-regulated kinase 1/2. We also demonstrate that the FasL ICD interacts with the transcription factor lymphoid-enhancer binding factor-1 and inhibits lymphoid-enhancer binding factor-1-dependent transcription. In vivo, plasma cell numbers, generation of germinal center B cells, and, consequently, production of antigen-specific immunoglobulin M antibodies in response to immunization with T cell-dependent or T cell-independent antigen are negatively affected in presence of the FasL ICD, suggesting that FasL reverse signaling participates in negative fine-tuning of certain immune responses. (Blood. 2011; 117(2):519-529) Show less