Intravenous immunoglobulin G (
IVIG) is used to treat
idiopathic thrombocytopenic purpura (
ITP). Although many patients benefit from
IVIG, some are refractory to this
therapy.
ITP is characterized by platelet clearance mediated primarily by antiplatelet
antibodies against GPIIbIIIa and/or the GPIbalpha complex. These 2 groups of
antibodies may induce
ITP through different mechanisms. We tested the hypothesis that
IVIG may not be equally effective in preventing
ITP caused by anti-GPIIbIIIa versus anti-GPIbalpha
antibodies in mice.
Thrombocytopenia was induced in BALB/c mice using
monoclonal antibodies against either mouse GPIIbIIIa (JON1, JON2, and JON3) or GPIbalpha (p0p3, p0p4, p0p5, p0p9, and p0p11). Pretreatment with
IVIG significantly ameliorated
ITP in all anti-GPIIbIIIa-injected animals. Conversely,
IVIG failed to prevent
ITP in all anti-GPIbalpha-treated mice, except for p0p4. These results were repeated in C57BL/6 mice, and with different
IVIG preparations. These data in mice suggest that patients with
ITP mediated by anti-GPIbalpha
antibodies may be less responsive to
IVIG treatment.