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B-
Develop Normally, But Have Selective Defects in Proliferation and Function1
,
,¶
Departments of
*
Microbiology and Immunology and
Cell Biology, Vanderbilt University School of Medicine, Nashville, TN 37232;
Howard Hughes Medical Institute, Chevy Chase, MD 20815;
Vanderbilt-Ingram Cancer Center, Nashville, TN 37232; and
¶ Transplantation and Immunobiology Section, Division of Allergy, Immunology, and Infectious Disease, National Institutes of Health, Bethesda, MD 20892
NF-
B has been implicated in the development, activation, and
function of B and T lymphocytes. We have evaluated the in vivo effects
of deletion of IB-
, a major inhibitor of NF-B, on lymphocyte
development, proliferation, and function. To elucidate the long term
role of IB- in lymphocytes, fetal liver cells of 14.5-day-old
IB--/- or wild-type embryos were transplanted into
irradiated recombinase-activating gene-2-deficient mice. Within 4 wk,
the IB--/- fetal liver cells reconstitute mature B
and T cell populations in the recipients comparable to those produced
by wild-type fetal liver cells. However, the proliferative responses of
IB--/- B cells are enhanced, whereas those of
IB--/- T cells are reduced. The levels of IgG1,
IgG2a, IgA, and IgE produced by IB--/- B cells are
elevated relative to those produced by IB-+/+ or
IB-+/-. Moreover, the specific immune
responses to OVA and the generation of germinal centers are impaired in
recipients of IB--/- fetal liver cells. These
results indicate that IB- plays a vital role in signal
transduction pathways regulating lymphocyte proliferation and also in
the production of specific Ig isotypes.
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