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Blood, 1 April 2006, Vol. 107, No. 7, pp. 2613-2618.
Prepublished online as a Blood First Edition Paper on November 29, 2005; DOI 10.1182/blood-2005-07-2965.
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CHEMOKINES, CYTOKINES, AND INTERLEUKINS
Upon viral exposure, myeloid and plasmacytoid dendritic cells produce 3 waves of distinct chemokines to recruit immune effectors
Bernard Piqueras,
John Connolly,
Heidi Freitas,
Anna Karolina Palucka, and
Jacques Banchereau
From the Baylor NIAID (National Institute of Allergy and Infectious Disease) Cooperative Center for Translational Research on Human Immunology and Biodefense, and Baylor Institute for Immunology Research, Dallas, TX.
Host response to viral infection involves distinct effectors of innate and adaptive immunity, whose mobilization needs to be coordinated to ensure protection. Here we show that influenza virus triggers, in human blood dendritic-cell (DC) subsets (ie, plasmacytoid and myeloid DCs), a coordinated chemokine (CK) secretion program with 3 successive waves. The first one, occurring at early time points (2 to 4 hours), includes CKs potentially attracting effector cells such as neutrophils, cytotoxic T cells, and natural killer (NK) cells (CXCL16, CXCL1, CXCL2, and CXCL3). The second one occurs within 8 to 12 hours and includes CKs attracting effector memory T cells (CXCL8, CCL3, CCL4, CCL5, CXCL9, CXCL10, and CXCL11). The third wave, which occurs after 24 to 48 hours, when DCs have reached the lymphoid organs, includes CCL19, CCL22, and CXCL13, which attract naive T and B lymphocytes. Thus, human blood DC subsets carry a common program of CK production, which allows for a coordinated attraction of the different immune effectors in response to viral infection.

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