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Abnormal lymphokine production: a novel feature of the genetic disease
Fanconi anemia. II. In vitro and in vivo spontaneous overproduction of
tumor necrosis factor alpha
F Rosselli, J Sanceau, E Gluckman, J Wietzerbin and E Moustacchi
URA 1292 du CNRS, Institut Curie-Biologie, Paris, France.
We have previously shown an unbalanced cytokine production in Fanconi
anemia (FA) cells, ie, an underproduction of interleukin 6 (IL-6) during
growth. Among a number of cytokines analyzed, the only other anomalies
detected concern tumor necrosis factor alpha (TNF alpha). In comparison to
normal cells, this cytokine is overproduced by FA lymphoblasts from the
four genetic complementation groups. Indeed, up to an eight-fold increase
in TNF alpha is observed in the growth medium of FA cells. Moreover,
addition of anti-TNF alpha antibodies partially corrects the FA
hypersensitivity to treatment by mitomycin C (MMC). Treatment of FA cells
with IL-6, which partially restored an almost normal sensitivity to MMC of
FA cells also reduces the TNF alpha overproduction in FA lymphoblasts. No
anomalies at the molecular level (Southern and Northern blot analyses) are
detected for the TNF alpha gene and its mRNA. We have investigated the in
vivo situation by assaying TNF alpha levels in the serum from FA
homozygotes and obligate heterozygotes. In contrast to normal healthy
donors or to aplastic anemia patients in whom serum TNF alpha is present
only in trace amounts, all 36 FA patients and 21 FA parents monitored show
a significantly (P < .001) higher level of serum TNF alpha activity.
Consequently, abnormal TNF alpha production seems to be associated with the
FA genetic background.
Volume 83,
Issue 5,
pp. 1216-1225,
03/01/1994
Copyright © 1994 by The American Society of Hematology
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