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Lymphokine abnormalities in aplastic anemia: implications for the mechanism
of action of antithymocyte globulin
P Gascon, NC Zoumbos, G Scala, JY Djeu, JG Moore and NS Young
Anti-thymocyte globulin (ATG) provides effective therapy for many patients
with aplastic anemia, and its mechanism of action has been presumed to be
secondary to lymphocytotoxicity. However, our studies of lymphocyte
function in aplastic anemia show marked abnormalities of lymphokine
production, which ATG may modulate. In 12 of 17 patients with aplastic
anemia, interleukin 2 (IL2) production was markedly elevated in vitro (P
less than .01 by paired statistical analysis). Expression of the IL2
receptor, or Tac antigen, on peripheral lymphocytes assessed by flow
microfluorometry was also increased above the normal range in 11 of 15
cases. Studies of ATG suggested that it might act to stimulate lymphocyte
function. In vitro, ATG is a mitogen, as measured by incorporation of
3H-thymidine into blood mononuclear cells; the response of cells to ATG
from patients with aplastic anemia was exaggerated in comparison with
normals. Cell proliferation was accompanied by production of IL2 to levels
that were, in some cases, similar to those obtained with lectin
stimulation. Finally, supernatants from lymphocytes cultured in the
presence of ATG were able to replace adherent cells in providing growth
factors for the support of nonadherent cells in methylcellulose
hematopoietic colony assays. These results provide a mechanism for an
"immunostimulatory" action of ATG in effecting hematopoietic response in
some patients with aplastic anemia.
Volume 65,
Issue 2,
pp. 407-413,
02/01/1985
Copyright © 1985 by The American Society of Hematology
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