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Increased antiplatelet T helper lymphocyte reactivity in patients with
autoimmune thrombocytopenia
JW Semple and J Freedman
Department of Immunohematology, St Michael's Hospital, Toronto, Ontario,
Canada.
Chronic autoimmune thrombocytopenic purpura (ATP) is a common hematologic
disorder in which platelet-specific autoantibodies bind to platelets and
enhance their destruction by the reticuloendothelial system. While there
has been considerable investigation of the humoral immune abnormalities in
ATP, little work has been performed on the cellular immunoregulatory
aspects of this autoimmune disorder. We describe here that patients with
ATP have lymphocytes that proliferate normally when stimulated by mitogens.
However, when stimulated by normal control platelets in 7-day
antigen-presenting cell cultures, peripheral blood mononuclear cells (PBMC)
from patients with ATP proliferate at significantly higher levels (P less
than .001) and their lymphocytes secrete significantly higher amounts of
interleukin-2 (IL- 2) (P less than .001) than do lymphocytes from control
subjects. Depletion studies with monoclonal anti-CD8 and complement did not
reduce the proliferative capacity of the responding PBMC population,
indicating that CD4+ T-helper cells may be responsible for the response.
Phenotypic analysis of peripheral blood lymphocyte subsets from patients
with ATP showed that there was a significant reduction in CD4+Leu8+ T
suppressor-inducer cells (P less than .001) and a concomitant increase in
CD3+DR+ activated T cells (P less than .001) and CD19+ B cells (P less than
.05). These data indicate that CD4+ T- helper cells from patients with ATP
are stimulated by normal platelet antigen(s) to secrete IL-2 and may
modulate the enhanced antiplatelet autoantibody response.
Volume 78,
Issue 10,
pp. 2619-2625,
11/15/1991
Copyright © 1991 by The American Society of Hematology
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