SignificanceWhile electronic states with nontrivial topology have traditionally been known in insulators, they have been evidenced in metals during the past 2 years. Such Weyl semimetals show topological protection while conducting electricity both in the bulk and on the surface. An outstanding question is whether topological protection can happen in metals with strong correlations. Here, we report theoretical work on a strongly correlated lattice model to demonstrate the emergence of a Weyl–Kondo semimetal. We identify Weyl fermions in the bulk and Fermi arcs on the surface, both of which are associated with the many-body phenomenon called the Kondo effect. We determine a key signature of this Weyl–Kondo semimetal, which is realized in a recently discovered heavy-fermion compound.

We demonstrate that the entanglement entropy area law for free fermion ground states and the corresponding volume law for highly excited states are related by a position-momentum duality, thus of the same origin. For a typical excited state in the thermodynamic limit, we further show that the reduced density matrix of a subsystem approaches thermal density matrix, provided the subsystem's linear size is small compared to that of the whole system in all directions, a property we dub eigenstate typicality. This provides an explicit example of thermalization via entanglement, and reveals how statistical physics emerges from a single eigenstate by tracing out a large number of degrees of freedom.

Mesenchymal stem/stromal cells (MSCs) are promising potential candidates for the treatment of immunological diseases because of their immunosuppressive functions. However, the molecular mechanisms that mediate MSCs’ immunosuppressive activity remain elusive. In this article, we report for the first time, to our knowledge, that secreted growth-regulated oncogene (GRO) chemokines, specifically GRO-γ, in human MSC-conditioned media have an effect on the differentiation and the function of human monocyte-derived dendritic cells. The monocyte-derived dendritic cells were driven toward a myeloid-derived suppressor cell (MDSC)–like phenotype by the GRO chemokines. GRO-γ–treated MDSCs had a tolerogenic phenotype that was characterized by an increase in the secretion of IL-10 and IL-4, and a reduction in the production of IL-12 and IFN-γ. We have also shown that the mRNA expression levels of the arginase-1 and inducible NO synthase genes, which characterize MDSCs, were upregulated by GRO-γ–primed mouse bone marrow cells. In addition, the ability of GRO-γ–treated bone marrow–derived dendritic cells to stimulate the OVA-specific CD8+ T (OT-1) cell proliferation and the cytokine production of IFN-γ and TNF-α were significantly decreased in vivo. Our findings allow a greater understanding of how MDSCs can be generated and offer new perspectives to exploit the potential of MDSCs for alternative approaches to treat chronic inflammation and autoimmunity, as well as for the prevention of transplant rejection.