Erythrocyte Receptors for (
            <i>Plasmodium Knowlesi</i>
            ) Malaria: Duffy Blood Group Determinants

Miller, Louis H.; Mason, Steven J.; Dvorak, James A.; McGinniss, Mary H.; Rothman, Ivan

doi:10.1126/science.1145213

Cited by 571 publications

(363 citation statements)

References 11 publications

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“…An example of infection shaping the human genome was provided by the discovery of Mendelian resistance to Plasmodium vivax (1,2). It is important to stress here that these studies concerned infection per se and not its manifestations ( Table 1).…”

Section: Mendelian Resistance To Malariamentioning

confidence: 99%

Severe infectious diseases of childhood as monogenic inborn errors of immunity

Casanova

2015

Proc. Natl. Acad. Sci. U.S.A.

201

163

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This paper reviews the developments that have occurred in the field of human genetics of infectious diseases from the second half of the 20th century onward. In particular, it stresses and explains the importance of the recently described monogenic inborn errors of immunity underlying resistance or susceptibility to specific infections. The monogenic component of the genetic theory provides a plausible explanation for the occurrence of severe infectious diseases during primary infection. Over the last 20 y, increasing numbers of life-threatening infectious diseases striking otherwise healthy children, adolescents, and even young adults have been attributed to single-gene inborn errors of immunity. These studies were inspired by seminal but neglected findings in plant and animal infections. Infectious diseases typically manifest as sporadic traits because human genotypes often display incomplete penetrance (most genetically predisposed individuals remain healthy) and variable expressivity (different infections can be allelic at the same locus). Infectious diseases of childhood, once thought to be archetypal environmental diseases, actually may be among the most genetically determined conditions of mankind. This nascent and testable notion has interesting medical and biological implications.

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Section: Mendelian Resistance To Malariamentioning

confidence: 99%

Severe infectious diseases of childhood as monogenic inborn errors of immunity

Casanova

2015

Proc. Natl. Acad. Sci. U.S.A.

201

163

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“…The lack of signaling by these receptors is ascribed either to the complete absence of the DRYLAIV motif, as is the case for DARC, or to the presence of presumably nonfunctional modified forms of this motif (DKYLEIV in D6, DRY-VAVT in CCX-CKR1, and DRYLSIT in CXCR7) (23). DARC was first discovered on RBCs as the Duffy blood group Ag (24) and was subsequently shown to serve as a receptor for the malarial parasites Plasmodium vivax and Plasmodium knowlesi (25,26). DARC has been established as a promiscuous chemokine receptor that can bind several chemokines, including CXCL1, to which it binds with the highest affinity (27).…”

mentioning

confidence: 99%

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

Al-Alwan

Chang

Rousseau

et al. 2014

The Journal of Immunology

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Airway smooth muscle cell (ASMC) migration is an important mechanism postulated to play a role in airway remodeling in asthma. CXCL1 chemokine has been linked to tissue growth and metastasis. In this study, we present a detailed examination of the inhibitory effect of CXCL1 on human primary ASMC migration and the role of the decoy receptor, Duffy AgR for chemokines (DARC), in this inhibition. Western blots and pathway inhibitors showed that this phenomenon was mediated by activation of the ERK-1/2 MAPK pathway, but not p38 MAPK or PI3K, suggesting a biased selection in the signaling mechanism. Despite being known as a nonsignaling receptor, small interference RNA knockdown of DARC showed that ERK-1/2 MAPK activation was significantly dependent on DARC functionality, which, in turn, was dependent on the presence of heat shock protein 90 subunit α. Interestingly, DARC- or heat shock protein 90 subunit α–deficient ASMCs responded to CXCL1 stimulation by enhancing p38 MAPK activation and ASMC migration through the CXCR2 receptor. In conclusion, we demonstrated DARC’s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK–signaling pathway.

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“…Following on observations that vivax malaria was rare in Africa (6), Miller et al performed definitive in vivo studies to show that Duffy-negative people resisted, whereas Duffy-positive people were susceptible, to experimental P. vivax blood-stage infection following exposure to infected mosquitoes (7). This seminal work, and related Plasmodium knowlesi in vitro studies (7)(8)(9), established the paradigm that malaria parasites invade erythrocytes through specific "receptor"-based interactions and that the Duffy blood group was the receptor for P. vivax.…”

mentioning

confidence: 99%

Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people

Ménard

Barnadas

Bouchier

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

349

354

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Malaria therapy, experimental, and epidemiological studies have shown that erythrocyte Duffy blood group-negative people, largely of African ancestry, are resistant to erythrocyte Plasmodium vivax infection. These findings established a paradigm that the Duffy antigen is required for P. vivax erythrocyte invasion. P. vivax is endemic in Madagascar, where admixture of Duffy-negative and Duffy-positive populations of diverse ethnic backgrounds has occurred over 2 millennia. There, we investigated susceptibility to P. vivax blood-stage infection and disease in association with Duffy blood group polymorphism. Duffy blood group genotyping identified 72% Duffy-negative individuals (FY*B ES /*B ES ) in community surveys conducted at eight sentinel sites. Flow cytometry and adsorption-elution results confirmed the absence of Duffy antigen expression on Duffy-negative erythrocytes. P. vivax PCR positivity was observed in 8.8% (42/476) of asymptomatic Duffy-negative people. Clinical vivax malaria was identified in Duffy-negative subjects with nine P. vivax monoinfections and eight mixed Plasmodium species infections that included P. vivax (4.9 and 4.4% of 183 participants, respectively). Microscopy examination of blood smears confirmed blood-stage development of P. vivax, including gametocytes. Genotyping of polymorphic surface and microsatellite markers suggested that multiple P. vivax strains were infecting Duffy-negative people. In Madagascar, P. vivax has broken through its dependence on the Duffy antigen for establishing human blood-stage infection and disease. Further studies are necessary to identify the parasite and host molecules that enable this Duffyindependent P. vivax invasion of human erythrocytes.erythrocyte | evolution | DARC | Madagascar

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Erythrocyte Receptors for ( Plasmodium Knowlesi ) Malaria: Duffy Blood Group Determinants

Cited by 571 publications

References 11 publications

Severe infectious diseases of childhood as monogenic inborn errors of immunity

Severe infectious diseases of childhood as monogenic inborn errors of immunity

CXCL1 Inhibits Airway Smooth Muscle Cell Migration through the Decoy Receptor Duffy Antigen Receptor for Chemokines

Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people

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