Kyoto University

About: Kyoto University is a education organization based out in Kyoto, Japan. It is known for research contribution in the topics: Population & Catalysis. The organization has 85837 authors who have published 217215 publications receiving 6526826 citations. The organization is also known as: Kyōto University & Kyōto daigaku.

Dysfunctional Blood and Target Tissue CD4+CD25high Regulatory T Cells in Psoriasis: Mechanism Underlying Unrestrained Pathogenic Effector T Cell Proliferation

Abstract: The balance between regulatory and effector functions is important for maintaining efficient immune responses, while avoiding autoimmunity. The inflammatory skin disease psoriasis is sustained by the ongoing activation of pathogenic effector T cells. We found that a CD4+ T lymphocyte subpopulation in peripheral blood, phenotypically CD25high, CTLA-4+, Foxp3high (regulatory T (Treg) cells), is deficient in its suppressor activity in psoriasis. This was associated with accelerated proliferation of CD4+ responder T cells in psoriasis, the majority of which expressed CXCR3. Nevertheless, criss-cross experiments isolated the defect to psoriatic Treg cells. To examine Treg cells in a nonlymphoid tissue of a human T cell-mediated disease, Treg cells were also analyzed and isolated from the site of inflammation, psoriatic lesional skin. At the regulatory vs effector T cells ratios calculated to be present in skin, however, the psoriatic Treg cell population demonstrated decreased suppression of effector T cells. Thus, dysfunctional blood and target tissue CD4+CD25high Treg cell activity may lead to reduced restraint and consequent hyperproliferation of psoriatic pathogenic T cells in vivo. These findings represent a critical component of human organ-specific autoimmune disease and may have important implications with regard to the possible therapeutic manipulation of Treg cells in vivo.

Topological Phases of Non-Hermitian Systems

Abstract: Recent experimental advances in controlling dissipation have brought about unprecedented flexibility in engineering non-Hermitian Hamiltonians in open classical and quantum systems. A particular interest centers on the topological properties of non-Hermitian systems, which exhibit unique phases with no Hermitian counterparts. However, no systematic understanding in analogy with the periodic table of topological insulators and superconductors has been achieved. In this paper, we develop a coherent framework of topological phases of non-Hermitian systems. After elucidating the physical meaning and the mathematical definition of non-Hermitian topological phases, we start with one-dimensional lattices, which exhibit topological phases with no Hermitian counterparts and are found to be characterized by an integer topological winding number even with no symmetry constraint, reminiscent of the quantum Hall insulator in Hermitian systems. A system with a nonzero winding number, which is experimentally measurable from the wave-packet dynamics, is shown to be robust against disorder, a phenomenon observed in the Hatano-Nelson model with asymmetric hopping amplitudes. We also unveil a novel bulk-edge correspondence that features an infinite number of (quasi-)edge modes. We then apply the K-theory to systematically classify all the non-Hermitian topological phases in the Altland-Zirnbauer classes in all dimensions. The obtained periodic table unifies time-reversal and particle-hole symmetries, leading to highly nontrivial predictions such as the absence of non-Hermitian topological phases in two dimensions. We provide concrete examples for all the nontrivial non-Hermitian AZ classes in zero and one dimensions. In particular, we identify a Z2 topological index for arbitrary quantum channels. Our work lays the cornerstone for a unified understanding of the role of topology in non-Hermitian systems.

Modulation of cell death by Bcl-XL through caspase interaction.

Abstract: The caspases are cysteine proteases that have been implicated in the execution of programmed cell death in organisms ranging from nematodes to humans. Many members of the Bcl-2 family, including Bcl-xL, are potent inhibitors of programmed cell death and inhibit activation of caspases in cells. Here, we report a direct interaction between caspases and Bcl-xL. The loop domain of Bcl-xL is cleaved by caspases in vitro and in cells induced to undergo apoptotic death after Sindbis virus infection or interleukin 3 withdrawal. Mutation of the caspase cleavage site in Bcl-xL in conjunction with a mutation in the BH1 homology domain impairs the death-inhibitory activity of Bcl-xL, suggesting that interaction of Bcl-xL with caspases may be an important mechanism of inhibiting cell death. However, once Bcl-xL is cleaved, the C-terminal fragment of Bcl-xL potently induces apoptosis. Taken together, these findings indicate that the recognition/cleavage site of Bcl-xL may facilitate protection against cell death by acting at the level of caspase activation and that cleavage of Bcl-xL during the execution phase of cell death converts Bcl-xL from a protective to a lethal protein.