Human XCL1 blocking peptide

Solid electrolytes with high ionic conductivity and good stability are advantageous over the current liquid electrolytes in rechargeable Li-ion batteries. Argyrodites, Li6PS5X (X = Cl, Br, or I), with ionic conductivities on the order of mS/cm have attracted tremendous attention. However, the high potential of argyrodites in fast ion conduction is far from being reached. Significant enhancement in ion conduction relies on the fundamental understanding of the contributing factors for fast ion transport. Here, we have systematically prepared highly conductive Li-deficient Li6-xPS5-xCl1+x and examined the influence of Li-deficiency and Cl substitution of S on ion transport using impedance spectroscopy, solid-state NMR, and first-principles calculations. With increased Cl content, the amount of Cl- at S2- (4d) sites increases, forming a dominant 1S3Cl (4d) configuration. In addition, Li+ redistributes with significantly higher mobility. As a result, the activation energy for Li-ion transport decreases, and the conductivity increases to 17 mS/cm at 25 degrees C when x equals 0.7 (Li5.3PS4.3Cl1.7). This work not only reports a record ionic conductivity of Cl-containing argyrodites-type fast Li-ion conductors, but also provides new insights into anion disorder-induced ion transport, which has a wide and universal appeal in the development of fast ion conductors and mixed-anion functional materials.

Background Every year, millions of people suffer from various forms of traumatic brain injury (TBI), and new approaches with therapeutic potential are required. Although chemokines are known to be involved in brain injury, the importance of X-C motif chemokine ligand 1 (XCL1) and its receptors, X-C motif chemokine receptor 1 (XCR1) and alpha-9 integrin (ITGA9), in the progression of TBI remain unknown. Methods Using RT-qPCR/Western blot/ELISA techniques, changes in the mRNA/protein levels of XCL1 and its two receptors, in brain areas at different time points were measured in a mouse model of TBI. Moreover, their cellular origin and possible changes in expression were evaluated in primary glial cell cultures. Results Studies revealed the spatiotemporal upregulation of the mRNA expression of XCL1, XCR1 and ITGA9 in all the examined brain areas (cortex, thalamus, and hippocampus) and at most of the evaluated stages after brain injury (24 h; 4, 7 days; 2, 5 weeks), except for ITGA9 in the thalamus. Moreover, changes in XCL1 protein levels occurred in all the studied brain structures; the strongest upregulation was observed 24 h after trauma. Our in vitro experiments proved that primary murine microglial and astroglial cells expressed XCR1 and ITGA9, however they seemed not to be a main source of XCL1. Conclusions These findings indicate that the XCL1/XCR1 and XCL1/ITGA9 axes may participate in the development of TBI. The XCL1 can be considered as one of the triggers of secondary injury, therefore XCR1 and ITGA9 may be important targets for pharmacological intervention after traumatic brain injury.