{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T17:36:22Z","timestamp":1774114582523,"version":"3.50.1"},"reference-count":27,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"5125","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[1993,8,27]]},"abstract":"<jats:p>\n            <jats:italic>Plasmodium vivax<\/jats:italic>\n            and\n            <jats:italic>P. falciparum<\/jats:italic>\n            are the major causes of human malaria, except in sub-Saharan Africa where people lack the Duffy blood group antigen, the erythrocyte receptor for\n            <jats:italic>P. vivax<\/jats:italic>\n            . Duffy negative human erythrocytes are resistant to invasion by\n            <jats:italic>P. vivax<\/jats:italic>\n            and the related monkey malaria,\n            <jats:italic>P. knowlesi<\/jats:italic>\n            . Several lines of evidence in the present study indicate that the Duffy blood group antigen is the erythrocyte receptor for the chemokines interleukin-8 (IL-8) and melanoma growth stimulatory activity (MGSA). First, IL-8 binds minimally to Duffy negative erythrocytes. Second, a monoclonal antibody to the Duffy blood group antigen blocked binding of IL-8 and other chemokines to Duffy positive erythrocytes. Third, both MGSA and IL-8 blocked the binding of the parasite ligand and the invasion of human erythrocytes by\n            <jats:italic>P. knowlesi<\/jats:italic>\n            , suggesting the possibility of receptor blockade for anti-malarial therapy.\n          <\/jats:p>","DOI":"10.1126\/science.7689250","type":"journal-article","created":{"date-parts":[[2006,10,5]],"date-time":"2006-10-05T23:05:09Z","timestamp":1160089509000},"page":"1182-1184","source":"Crossref","is-referenced-by-count":481,"title":["A Receptor for the Malarial Parasite\n            <i>Plasmodium vivax<\/i>\n            : the Erythrocyte Chemokine Receptor"],"prefix":"10.1126","volume":"261","author":[{"given":"Richard","family":"Horuk","sequence":"first","affiliation":[{"name":"Genentech, Inc., South San Francisco, CA 94080."}]},{"given":"Chetan E.","family":"Chitnis","sequence":"additional","affiliation":[{"name":"Laboratory of Malaria Research, National Institutes of Health, Bethesda, MD 20892."}]},{"given":"Walter C.","family":"Darbonne","sequence":"additional","affiliation":[{"name":"Genentech, Inc., South San Francisco, CA 94080."}]},{"given":"Timothy J.","family":"Colby","sequence":"additional","affiliation":[{"name":"Genentech, Inc., South San Francisco, CA 94080."}]},{"given":"Anne","family":"Rybicki","sequence":"additional","affiliation":[{"name":"Montefiore Medical Center, Bronx, NY 10467."}]},{"given":"Terence J.","family":"Hadley","sequence":"additional","affiliation":[{"name":"Division of Medical Oncology\/Hematology, J. G. Brown Cancer Center, Louisville, KY 40292."}]},{"given":"Louis H.","family":"Miller","sequence":"additional","affiliation":[{"name":"Laboratory of Malaria Research, National Institutes of Health, Bethesda, MD 20892."}]}],"member":"221","reference":[{"key":"e_1_2_1_1_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.1334571"},{"key":"e_1_2_1_2_1","first-page":"CH5","volume":"1","year":"1987","unstructured":"Bradley, D. 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