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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1370-1377
Both Stat5a and Stat5b are required for antigen-induced
eosinophil and T-cell recruitment into the tissue
Shin-ichiro Kagami,
Hiroshi Nakajima,
Kotaro Kumano,
Kotaro Suzuki,
Akira Suto,
Kazunori Imada,
Helen W. Davey,
Yasushi Saito,
Kiyoshi Takatsu,
Warren J. Leonard, and
Itsuo Iwamoto
From the Department of Internal Medicine II, Chiba University School
of Medicine, Chiba, Japan; Laboratory of Molecular Immunology, National
Heart, Lung, and Blood Institute, Bethesda, MD; AgResearch, Ruakura,
Hamilton, New Zealand; and Department of Immunology, Institute of
Medical Science, University of Tokyo, Japan.
Antigen-induced eosinophil recruitment into the airways of
sensitized mice is mediated by CD4+ T cells and their
cytokines, especially IL-5. In this study, we found that the
antigen-induced airway eosinophilia was diminished in Stat5a-deficient
(Stat5a /) mice and Stat5b-deficient
(Stat5b/) mice. We also found that antigen-induced
CD4+ T-cell infiltration and IL-5 production in the
airways were diminished in Stat5a/ mice and
Stat5b/ mice. Moreover, antigen-induced proliferation
of splenocytes was diminished in Stat5a/ mice and
Stat5b/ mice, suggesting that the generation of
antigen-primed T cells may be compromised in Stat5a/
mice and Stat5b/ mice and this defect may account for
the diminished antigen-induced T-cell infiltration into the airways.
Interestingly, IL-4 and IL-5 production from anti-CD3-stimulated
splenocytes was diminished in Stat5a/ mice and
Stat5b/ mice. However, antigen-specific IgE and IgG1
production was diminished in Stat5a/ mice but not in
Stat5b/ mice, whereas antigen-specific IgG2a
production was increased in Stat5a/ mice, suggesting
the enhanced Th1 responses in Stat5a/ mice. Finally,
we found that eosinophilopoiesis induced by the administration of
recombinant IL-5 was also diminished in Stat5a/ mice
and Stat5b/ mice. Together, these results indicate
that both Stat5a and Stat5b are essential for induction of
antigen-induced eosinophil recruitment into the airways and that the
defects in antigen-induced eosinophil recruitment in
Stat5a/ mice and Stat5b/ mice
result from both impaired IL-5 production in the airways and diminished
IL-5 responsiveness of eosinophils.
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