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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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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 Fc 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.

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