CXCR3

[Cell Reports] Scientists reported that pro-inflammatory β cell small extracellular vesicles induced β cell dysfunction, promoted a pro-inflammatory islet transcriptome, and enhanced recruitment of CD8+ T cells and macrophages.

[Journal of Clinical Investigation] Scientists showed that natural killer (NK)-cell suppression of T cells is associated with transient accumulation of NK cells within T cell-rich sites of the spleen during lymphocytic choriomeningitis virus infection.

[JCI Insight] Investigators showed that macrophages contributed significantly to the loss of β-cells and the subsequent development of hyperglycemia. Depletion or inhibition of 12-LOX in this model resulted in reduced macrophage infiltration into islets and the preservation of β-cell mass.

[Cell Metabolism] Scientists uncovered and characterized a distinct population of inflammatory hepatic CXCR3+Th17 (ihTh17) cells sufficient to exacerbate non-alcoholic fatty liver disease pathogenesis.

[Cell Metabolism] Scientists uncovered and characterized a distinct population of inflammatory hepatic CXCR3+Th17 cells sufficient to exacerbate non-alcoholic fatty liver disease pathogenesis.

[Communications Biology] Scientists showed that while AMD11070 acts as a full antagonist, plerixafor acts biased by stimulating β-arrestin recruitment while fully antagonizing G protein.