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 Blood, 1 August 2008, Vol. 112, No. 3, pp. 493-503.
Prepublished online as a Blood First Edition Paper on May 14, 2008; DOI 10.1182/blood-2007-08-108316.

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CHEMOKINES, CYTOKINES, AND INTERLEUKINS

Regulation of D6 chemokine scavenging activity by ligand- and Rab11-dependent surface up-regulation

Raffaella Bonecchi1,2,*, Elena M. Borroni1,2,*, Achille Anselmo1, Andrea Doni1, Benedetta Savino1,2, Massimiliano Mirolo1, Monica Fabbri3, Venkatakrishna R. Jala4, Bodduluri Haribabu4, Alberto Mantovani1,2, and Massimo Locati1,2

1 Istituto Clinico Humanitas, Istituti di ricovero e cura a carattere scientifico (IRCCS), Rozzano, Italy; 2 Istituto di Patologia Generale, University of Milan, Milan, Italy; 3 Unit of Leukocyte Biology, Department of Biological and Technological Research (DIBIT)-Scientific Institute San Raffaele, Milan, Italy; and 4 James Graham Brown Cancer Center, University of Louisville Health Sciences, KY

The decoy receptor D6 plays a nonredundant role in the control of inflammatory processes through scavenging of inflammatory chemokines. However it remains unclear how it is regulated. Here we show that D6 scavenging activity relies on unique trafficking properties. Under resting conditions, D6 constitutively recycled through both a rapid wortmannin (WM)–sensitive and a slower brefeldin A (BFA)–sensitive pathway, maintaining low levels of surface expression that required both Rab4 and Rab11 activities. In contrast to "conventional" chemokine receptors that are down-regulated by cognate ligands, chemokine engagement induced a dose-dependent BFA-sensitive Rab11-dependent D6 re-distribution to the cell membrane and a corresponding increase in chemokine degradation rate. Thus, the energy-expensive constitutive D6 cycling through Rab11 vesicles allows a rapid, ligand concentration–dependent increase of chemokine scavenging activity by receptor redistribution to the plasma membrane. D6 is not regulated at a transcriptional level in a variety of cellular contexts, thus ligand-dependent optimization of its scavenger performance represents a rapid and unique mechanism allowing D6 to control inflammation.


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A. Mantovani and M. Locati
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