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Prepublished online as a Blood First Edition Paper on October 10, 2002; DOI 10.1182/blood-2002-02-0620.

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2002-02-0620v1
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Blood, 15 February 2003, Vol. 101, No. 4, pp. 1419-1421

HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Brief report

Platelet activation induced by human antibodies to interleukin-8

Véronique Regnault, Emmanuel de Maistre, Jean-Pierre Carteaux, Yves Gruel, Philippe Nguyen, Brigitte Tardy, and Thomas Lecompte

From Hématologie, Faculté de Médecine, Nancy, France; Service d'Hématologie Biologique et Clinique de Chirurgie Cardio-vasculaire et Transplantation du Centre Hospitalier Universitaire (CHU) de Nancy, France; Service d'Hématologie-Hémostase du CHU A. Trousseau de Tours, France; EA 2070, Faculté de Médecine de Reims, France; Département d'Hématologie du CHU de Saint Etienne, France.

Some cases of heparin-induced thrombocytopenia (HIT) have been reported to be associated with antibodies against interleukin-8 (IL-8), a chemokine related to platelet factor 4. We found that sera from 5 HIT patients containing immunoglobulin G (IgG) or IgM antibodies to IL-8, as evidenced using surface plasmon resonance spectroscopy, were able to trigger IL-8-dependent activation of washed platelets, leading to procoagulant activity. This activation occurred at IL-8 concentrations achievable in vivo and was facilitated by heparin (0.1 U/mL). Activation was also induced by affinity-purified anti-IL-8 IgG and involved Fcgamma RIIa. In the 2 patients who could be followed up, antibodies were no longer detectable 4 months after heparin withdrawal. One additional patient with paraneoplastic recurrent thrombosis without thrombocytopenia was found to have platelet-activating anti-IL-8 IgM, but in this case heparin was inhibitory. This is another example of potentially pathogenic platelet activation by antibodies.

© 2003 by The American Society of Hematology.
 

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