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blood or cord blood, and independent of the use of T-cell depletion
[2,13]
.
Not only is the overall risk of infection greater following unrelated HSCT,
but it extends further post transplant, due to delayed immunological recov-
ery
[2,3,13-15]
. Studies of post-transplant immune recovery have examined
absolute lymphocyte counts, different lymphocyte subsets, as well as T-cell
repertoire and T-cell receptor expressing circles (TREC), which can be used
as markers of thymopoiesis
[2-5,16-21]
. A readily available clinical parame-
ter such as the absolute lymphocyte count (ALC) has been demonstrated to
be predictive of overall survival and relapse
[17-20]
. The risk of opportunis-
tic infections in the post-transplant period is correlated with the recovery of
T cells, and delayed reconstitution of CD4
+
T-cell counts correlates with an
increased risk of fatal opportunistic infections
[2,16]
.
A number of factors are thought to affect immune reconstitution, including
advanced patient age, the radiation and chemotherapy used in condition-
ing regimen, the use of
in vitro
or
in vivo
T-cell depletion to decrease GVHD,
HLA disparity between donor and recipient, and drugs used to prevent or
treat GVHD, as well as the occurrence of GVHD. The use of total body irra-
diation (TBI), commonly used in the conditioning regimen, decreases the
124
FIGURE 6.1
Strategies to improve post-transplant immunity. Abbreviations: PTH: parathyroid hormone; GH: growth hormone; TEC: Thymic epithelial cells. See text for other abbreviations.
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