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J Heyd, AD Donnenberg, WH Burns, R Saral and GW Santos
Johns Hopkins Oncology Center, Bone Marrow Transplantation Program,
Baltimore, MD.
Markedly elevated serum IgE levels have been noted following allogeneic
bone marrow transplantation (BMT) and have been correlated with graft-v-
host disease (GVHD) in several studies. To investigate this phenomenon, we
measured serum IgE levels in 387 allogeneic, 143 autologous, and 21
syngeneic BMT recipients before and at intervals after BMT. As a
population, allogeneic BMT recipients displayed a biphasic elevation in IgE
levels, with peak levels occurring either early (days 15 to 19) or late
(days 80 to 89) posttransplant. Only in individuals in whom peak levels
occurred early did IgE level correlate with liver disease, histological
changes, and overall clinical stage of GVHD. The association of IgE
elevation and GVHD does not appear to be direct since recipients of
syngeneic (monozygotic twin) grafts had the highest incidence of IgE
hyperresponsiveness as well as the highest absolute IgE levels. Similarly,
22 recipients of autologous marrow not treated with
4-hydroperoxycyclophosphamide had elevated IgE levels comparable to those
seen in allogeneic graft recipients. We hypothesize that augmented IgE
synthesis and its subsequent resolution is the natural consequence of
immune reconstitution in the presence of potentially reaginic agents such
as antibiotics and infectious agents. As such, IgE hyperresponsiveness in
syngeneic graft recipients may reflect the maturational sequence of IgE
regulatory elements in the absence of interference by GVHD, GVHD therapy,
or minor histocompatibility disparities. The cell populations required for
IgE response (T cells, B cells, and antigen-presenting cells) may be
reconstituted in advance of the regulatory elements that limit IgE
production in healthy subjects. Although this temporal relationship does
not appear to hold in allogeneic BMT, the balance between positive and
negative factors, which determines the rates of IgE synthesis and
catabolism, may be altered by GVHD, infection, and liver dysfunction acting
alone or in combination.
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| Copyright © 1988 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||