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*
National Institute of Immunology, New Delhi, India; and
Regional Medical Research Center, Bhubaneswar, India
We show that macrophages of X-linked immunodeficient mice with a
mutant nonfunctional Bruton’s tyrosine kinase produce less NO than
wild-type macrophages in response to a variety of stimuli. Induction of
the inducible NO synthase (iNOS) protein, the transcription factor IFN
regulatory factor-1 involved in iNOS expression, and the transcription
factor STAT-1 involved in regulating IFN regulatory factor-1 induction
are all poorer in X-linked immunodeficient than in wild-type
macrophages. On the other hand, induction of IL-12 is higher in
X-linked immunodeficient than in wild-type macrophages. Macrophage
IL-12 induction is enhanced by iNOS inhibitors such as aminoguanidine
and thiocitrulline and is inhibited by NO generation via sodium
nitroprusside. There is relative enhancement of IFN-
production by
immune T cells from mice immunized under aminoguanidine cover. Our data
thus suggest that Bruton’s tyrosine kinase participates in signaling
for iNOS induction via IFN regulatory factor-1 in macrophages and that
NO is an inhibitor of IL-12 induction.
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