During chronic viral infection, virus-specific CD8(+) T cells become exhausted, exhibit poor effector function and lose memory potential. However, exhausted CD8(+) T cells can still contain viral replication in chronic infections, although the mechanism of this containment is largely unknown. Here we show that a subset of exhausted CD8(+) T cells expressing the chemokine receptor CXCR5 has a critical role in the control of viral replication in mice that were chronically infected with lymphocytic choriomeningitis virus (LCMV). These CXCR5(+) CD8(+) T cells were able to migrate into B-cell follicles, expressed lower levels of inhibitory receptors and exhibited more potent cytotoxicity than the CXCR5(-) [corrected] subset. Furthermore, we identified the Id2-E2A signalling axis as an important regulator of the generation of this subset. In patients with HIV, we also identified a virus-specific CXCR5(+) CD8(+) T-cell subset, and its number was inversely correlated with viral load. The CXCR5(+) subset showed greater therapeutic potential than the CXCR5(-) [corrected] subset when adoptively transferred to chronically infected mice, and exhibited synergistic reduction of viral load when combined with anti-PD-L1 treatment. This study defines a unique subset of exhausted CD8(+) T cells that has a pivotal role in the control of viral replication during chronic viral infection.

Reconfigurable intelligent surfaces (RISs) comprised of tunable unit cells have recently drawn significant attention due to their superior capability in manipulating electromagnetic waves. In particular, RIS-assisted wireless communications have the great potential to achieve significant performance improvement and coverage enhancement in a cost-effective and energy-efficient manner, by properly programming the reflection coefficients of the unit cells of RISs. In this paper, free-space path loss models for RIS-assisted wireless communications are developed for different scenarios by studying the physics and electromagnetic nature of RISs. The proposed models, which are first validated through extensive simulation results, reveal the relationships between the free-space path loss of RIS-assisted wireless communications and the distances from the transmitter/receiver to the RIS, the size of the RIS, the near-field/far-field effects of the RIS, and the radiation patterns of antennas and unit cells. In addition, three fabricated RISs (metasurfaces) are utilized to further corroborate the theoretical findings through experimental measurements conducted in a microwave anechoic chamber. The measurement results match well with the modeling results, thus validating the proposed free-space path loss models for RIS, which may pave the way for further theoretical studies and practical applications in this field.

Stretchable, transparent nanogenerator enabled by ionic hydrogel converts motion energy into electricity and senses touch pressure.

Rheumatoid arthritis is a common chronic inflammatory disorder and a major cause of disability. Despite the progress made with recent clinical use of anti-cytokine biologics, the response rate of rheumatoid arthritis treatment remains unsatisfactory, owing largely to the complexity of cytokine interactions and the multiplicity of cytokine targets. Here, we show a nanoparticle-based broad-spectrum anti-inflammatory strategy for rheumatoid arthritis management. By fusing neutrophil membrane onto polymeric cores, we prepare neutrophil membrane-coated nanoparticles that inherit the antigenic exterior and associated membrane functions of the source cells, which makes them ideal decoys of neutrophil-targeted biological molecules. It is shown that these nanoparticles can neutralize proinflammatory cytokines, suppress synovial inflammation, target deep into the cartilage matrix, and provide strong chondroprotection against joint damage. In a mouse model of collagen-induced arthritis and a human transgenic mouse model of arthritis, the neutrophil membrane-coated nanoparticles show significant therapeutic efficacy by ameliorating joint damage and suppressing overall arthritis severity.