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CA Pugsley, IJ Forbes and AA Morley
The immunology of chronic hypoplastic marrow failure (CHMF, aplastic
anemia) was studied in an experimental murine model of the disease induced
by busulfan. B lymphocytes of peripheral blood, spleen, and bone marrow
were reduced to 30%-40% and T lymphocytes of thymus, spleen, marrow, and
blood were decreased to 20%-70% of control values. IgG and IgM antibody
titer to sheep red blood cells were reduced to one- third of control
levels, and splenic IgG, but not IgM, plaque-forming cells were fewer on
day 7 after antigen stimulation. The proliferative responses to
phytohemagglutinin or concanavalin A were reduced in cultures of peripheral
blood lymphocytes, splenic lymphocytes, and thymocytes, and cutaneous
delayed-type hypersensitivity induced by dinitrofluorobenze was not
detected in mice with CHMF. The results demonstrate disturbance of a
variety of cellular and humoral functions and suggest that the disturbance
was due to quantitative and possibly qualitative abnormalities of the cell
types subserving these functions. The results suggest that residual cell
injury, the lesion underlying experimental CHMF, is not confined to the
myeloid stem cell but also involved cells of the lymphoid series.
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