The use of multi-chemokine receptor reporter mice helps to unravel the dynamics of receptor involvement in leukocyte migration in vivo and suggests specificity, rather than redundancy, in receptor use.

Cell biological approaches and spatiotemporally resolved proteome profiling demonstrate that the chemokine receptor CCR7 can activate G proteins after being internalized into endosomes, from where it regulates Rac1-dependent chemotaxis.

A new form of chemokine signaling bias that depends on cell state is identified.

Experimentally validated structural models of ACKR1-LukE and CCR5-LukE complexes reveal the critical contributions of sulfotyrosine binding sites and divergent loops of Staphylococcus aureus leukotoxins to the recognition of chemokine receptors.

Numerous chemokine variants bearing no sequence resemblance elicit similar signaling behavior from the viral GPCR US28, suggesting a mechanism for receptor activation that accommodates extensive ligand degeneracy.

Combining particle tracking in living cells with statistical analysis demonstrates how the oligomeric organization of cell surface receptor influences their function, a necessary step in the development of drugs targeting specific receptor conformation.

In a new mechanism of cellular communication termed “inverse signaling", a transmembrane chemokine acts as a "receptor" for its previously shed form.

Two-photon microscopy, combined with chemotaxis assays, synchronized thymocyte selection studies, and flow cytometry analyses, reveal that CCR4 and CCR7 promote medullary entry and central tolerance of immature and mature post-positive selection thymocyte subsets, respectively, with distinct outcomes for central tolerance.

Key functional variants, discovered using Massively Parallel Reporter Assay (MPRA) and reporter assays in the context of SARS-CoV-2 infection, support the importance of two critical chemokine receptor genes CCR1 and CCR5 in severe Covid-19 illness.

Multiple biochemical assays show that the topology of CCR5 and possibly other GPCRs may be inverted by ceramide or other sphingolipids through the process of regulated alternative translocation.