Blood, Vol. 96 No. 2 (July 15), 2000:
pp. 783-783
ERRATUM
In the article by Anderson et al entitled
"Immunization of allogeneic bone marrow transplant recipients with
tumor cell vaccines enhances graft-versus-tumor activity without
exacerbating graft-versus-host disease," which appeared in the April
1, 2000, issue of Blood (95:2426-2433), the key legends from
Figures 1, 8, 9, and 10 were omitted. The figures are published below
in their entirety.
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| Fig 1.
Immunization of BMT recipients increases survival and GVT
activity.
One month after BMT, SW B6 recipients were immunized with 205IL-2/TK
cells and ganciclovir. Two weeks after the first vaccine,
micrometastases were established by intravenous injection of
1 × 105 205 tumor cells, at which time 1 group of
recipients received a second vaccine. Lung nodules were counted at the
time of death or after day 100 for each recipient. The deaths that
occurred in the recipient group immunized twice resulted from the
growth of a nonpulmonary metastasis (sacral/pelvic mass) that
necessitated sacrifice. Groups and sizes were: no vaccine, n = 4; 1 vaccine, n = 5; and 2 vaccines, n = 5. *P < .05 for
lung nodules compared to 1 or no vaccine controls. **P = .004
compared to nonimmunized recipient survival.
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| Fig 8.
Tumor immunization of BMT recipients increases antitumor
cytolytic activity and induces limited alloreactivity compared to
immune C3H.SW controls.
Three months (A) or 1 month (B, C) after BMT, C3H.SW B6 recipients
were immunized twice with irradiated 205IL-2/TK cells (205-immune) or
irradiated C1498 leukemia cells (C1498-immune) at a 1-week interval.
Control C3H.SW donors were also immunized in an identical manner. Ten
days after the 2nd vaccine, spleens were harvested, and spleen cells
were stimulated for 4 days in vitro with irradiated 205 (A, B) or C1498
(C). A 51Cr-release assay was performed using targets
specified in the legends. B6 CAB are C57BL/6 ConA lymphoblasts. A, B,
and C represent independent experiments with different panels of
targets; neither P815 nor Yac cells were used as targets in experiment
C because other experiments had demonstrated little or no LAK or NK
activity. Data shown are at an E:T ratio of 200:1, and each
effector:target condition was performed in triplicate using splenocytes
pooled from 2 or 3 mice.
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| Fig 9.
Tumor immunization of
C3H.SW BMT donors induces a
response to the mHAg
B6dom1 found on all
C57BL/6 tumor targets tested. C3H.SW (donor
strain) mice were immunized twice with 5 × 106
irradiated 205IL-2/TK cells (205-immune) or
20 × 106 C57BL/6 spleen cells (B6-immune) at a
weekly interval, or they were not immunized (naïve). Ten days
after the 2nd vaccine, their splenocytes were stimulated
for 5 days in vitro with C3H.SW spleen cells loaded exogenously with
B6dom1 peptide. A 51Cr-release assay was
performed using the targets specified in the graphs.
B6dom1/SW CAB indicates C3H.SW ConA lymphoblast targets
that were loaded exogenously with B6dom1 peptide, whereas
SW CAB were not loaded with peptide. Data shown are at an E:T
ratio of 100:1, and each effector:target condition was performed in
triplicate using splenocytes pooled from 2 or 3 mice. Panels A
and B represent data from the same experiment.
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| Fig 10.
Unresponsiveness to the recipient mHAg
B6dom1 is not reversed by post-transplant tumor
immunization of recipients.
One month after BMT, allogeneic BMT recipients or control C3H.SW donors
were immunized twice with irradiated 205IL-2/TK cells at a 1-week
interval. Ten days after the second vaccine, their splenocytes were
stimulated for 5 days in vitro with B6dom1-loaded C3H.SW
spleen cells. A 51Cr-release assay was then performed using
C3H.SW ConA lymphoblast targets that were either loaded with
B6dom1 peptide (B6dom1/SW CAB) or not loaded
with peptide (SW CAB). Data shown are at an E:T ratio of 50:1, and each
effector:target condition was performed in triplicate using splenocytes
pooled from 2 or 3 mice.
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