A role of the Duffy antigen for the maintenance of plasma chemokine concentrations.

Fukuma N, Akimitsu N, Hamamoto H, Kusuhara H, Sugiyama Y, Sekimizu K.

Laboratory of Developmental Biochemistry, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 3-1,
7-Chome, Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
We examined plasma chemokine concentrations and chemokine clearance rates in Duffy antigen knockout mice. The
plasma concentrations of eotaxin and MCP-1 in Duffy antigen knockout mice were less than one-third of those in wild-type
mice. When eotaxin or hMGSA was intravenously injected, the chemokine disappeared more rapidly from the plasma of
Duffy antigen knockout mice than from the plasma of wild-type mice. The half-lives of hIP-10 and interferon-gamma,
which do not have an affinity for the Duffy antigen, in plasma were indistinguishable between Duffy antigen knockout mice
and wild-type mice. These results suggest that the Duffy antigen delays the disappearance of chemokines from the
plasma, resulting in the maintenance of plasma chemokine concentrations.

PMID: 12646177 [PubMed - indexed for MEDLINE]

2006: Langhi Dante M; Bordin José Orlando

Duffy blood group and malaria.
Hematology (Amsterdam, Netherlands) 2006;11(5):389-98.

Very important progress has been made over the last years in understanding the Duffy blood group system and its
complexity. The Duffy blood group antigen serves not only as blood group antigen, but also as a receptor for a family of
proinflammatory cytokines termed chemokines, and as a receptor for Plasmodium vivax malaria parasites. The Duffy
antigen has been termed the "Duffy Antigen Receptor for Chemokines" (DARC) or the Duffy chemokine receptor. DARC
might play a role as a scanvenger on the red blood cell surface to eliminate excess of toxic chemokines produced in some
pathologic situations [48]. Plasmodium vivax (P. vivax) causes approximately between 70 and 80 million cases of malaria
per year and is the most amply distributed human malaria in the world [51]. Individuals with the Duffy-negative
phenotype are resistant to P. vivax invasion, and the molecular mechanism that gives rise to the phenotype Fy(a - b - ) in
black individuals has been associated with a point mutation - 33TC expressed in homozigosity in the FYB allele [5].
Despite P. vivax be widespread throughout the tropical and subtropical world, it is absent from West Africa, where more
than 95% of the population is Duffy negative. Recently, this point mutation has been described in heterozigosity in the
FYA allele in others malaria endemic regions [7, 8], and until now we do not know if it confers a certain degree of
protection against P. vivax infection.

Anti-Fy6 reacts with specialized endothelial cells (littoral cells) lining the sinusoids in the red pulp of the spleen.

Purkinje cells of the cerebellum express the DARC