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Prepublished online as a Blood First Edition Paper on August 22, 2002; DOI 10.1182/blood-2002-07-2157.
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Blood, 15 January 2003, Vol. 101, No. 2, pp. 621-623
IMMUNOBIOLOGY
Brief report
Suppression of autoreactive T-cell response to glycoprotein
IIb/IIIa by blockade of CD40/CD154 interaction: implications for
treatment of immune thrombocytopenic purpura
Masataka Kuwana,
Yutaka Kawakami, and
Yasuo Ikeda
From the Institute for Advanced Medical Research and
Department of Internal Medicine, Keio University School of Medicine,
Tokyo, Japan.
The potential immunosuppressive effect of an anti-CD154
monoclonal antibody (mAb) on the pathogenic autoreactive T-cell
response was evaluated using an in vitro culture system with
glycoprotein IIb/IIIa (GPIIb/IIIa)-reactive T cells from
patients with immune thrombocytopenic purpura (ITP). The anti-CD154 mAb
did not inhibit T-cell proliferation, but suppressed anti-GPIIb/IIIa
antibody production, in bulk peripheral blood mononuclear cell cultures stimulated with GPIIb/IIIa. Repeated antigenic stimulation of GPIIb/IIIa-reactive CD4+ T-cell lines in the presence of
anti-CD154 mAb resulted in the loss of proliferative capacity and
helper function for promoting anti-GPIIb/IIIa antibody production.
These anergic T-cell lines showed a cytokine profile of low interferon
 and high interleukin 10 and suppressed anti-GPIIb/IIIa antibody
production. Our results indicate that blockade of the CD40/CD154
interaction induces generation of autoantigen-specific anergic
CD4+ T cells with regulatory function and could
be a therapeutic option for suppressing pathogenic autoimmune responses
in patients with ITP.
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