CXCR4 dimerization and beta-arrestin-mediated signaling account for the enhanced chemotaxis to CXCL12 in WHIM syndrome.

@article{Lagane2008CXCR4DA,
  title={CXCR4 dimerization and beta-arrestin-mediated signaling account for the enhanced chemotaxis to CXCL12 in WHIM syndrome.},
  author={Bernard Lagane and Ken Yan-Ching Chow and Karl Balabanian and Ang{\'e}lique Levoye and Julie Harriague and Thierry Planchenault and Françoise Baleux and Nathalie Gunera-Saad and Fernando Arenzana-Seisdedos and Françoise Bachelerie},
  journal={Blood},
  year={2008},
  volume={112 1},
  pages={34-44}
}
WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome is an immune deficiency linked in many cases to heterozygous mutations causing truncations in the cytoplasmic tail of CXC chemokine receptor 4 (CXCR4). Leukocytes expressing truncated CXCR4 display enhanced responses to the receptor ligand CXCL12, including chemotaxis, which likely impair their trafficking and contribute to the immunohematologic clinical manifestations of the syndrome. CXCR4 desensitization and… CONTINUE READING