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*
Department of Immunobiology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304; and
Schering Plough Research Institute, Schering Plough Corporation, Lafayette, NJ 07848
Previous studies have shown that the chronic inflammation observed
in the colon of IL-10-deficient (IL-10-/-) mice is
mediated by CD4+ Th1 T cells and is dependent on the
presence of IFN-
for its initial development. As CD4+ T
cells from IL-10-/- mice will cause colitis when
transferred into recombinase-activating gene (Rag)-deficient
recipients, we considered the possibility that the recipients’ NK
cells could be an important source of IFN- for the development of
colitis. Therefore, the ability of IL-10-/-
CD4+ T cells to cause colitis in Rag-deficient recipients
that had been depleted of NK cells was tested. Contrary to our
expectations, NK cell-depleted recipients of IL-10-/-
CD4+ T cells developed accelerated disease compared with
nondepleted recipients. Furthermore, CD4+ T cells from
normal mice (IL-10+/+) also caused colitis in NK
cell-depleted recipient mice, but not in nondepleted recipients. NK
cells inhibited effector CD4+CD45RBhigh T
cells, and subsequent experiments showed that this effect was dependent
on perforin. Thus NK cells can play an important role in
down-regulating Th1-mediated colitis by controlling the responses of
effector T cells to gut bacteria.
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