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,
,§,¶
*
Division of Developmental and Clinical Immunology, Departments of
Medicine,
Pediatrics, and
§
Microbiology, University of Alabama, and the
¶
Howard Hughes Medical Institute, Birmingham, AL 35294; and
||
Washington University Center for Immunology and Department of Pathology, St. Louis, MO 63110
Type I IFNs, IFN-
, -ß, and -
, are cytokine family members
with multiple immune response roles, including the promotion of cell
growth and differentiation. Conversely, the type I IFNs are potent
inhibitors of IL-7-dependent growth of early B lineage progenitors,
effectively aborting further B lineage differentiation at the pro-B
cell stage. Type I IFNs and ß function via receptor-mediated
activation of a Jak/Stat signaling pathway in which Stat-1 is
functionally important, because many IFN-induced responses are
abrogated in Stat-1-deficient mice. To the contrary, we show here that
the inhibition of IL-7-dependent B lymphopoiesis by IFN-ß is
unaffected in Stat-1-deficient mice. The present data indicate that the
type I IFNs can activate an alternative signaling pathway in which
neither Stat-1 nor phosphatidylinositol 3'-kinase are essential
components.
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