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B Activation in Tumor-Associated Macrophages1
*
Istituto di Ricerche Farmacologiche "Mario Negri," Milan, Italy;
Department of Biotechnology, University of Brescia, Brescia, Italy; and
Rega Institute for Medical Research, University of Leuven, Leuven, Belgium
IL-12 is a central cytokine in the activation of inflammation and
immunity and in the generation of Th1-type responses. Tumor-associated
macrophages (TAM) from mouse and human tumors showed defective
production of IL-12. Defective IL-12 production was associated with
lack of p50/p65 NF-
B activation. TAM produced increased amounts of
the immunosuppressive cytokine IL-10. Abs against IL-10 restored the
defective capacity of TAM to produce IL-12. Our data suggest that
during tumor growth an IL-10-dependent pathway of diversion of
macrophage function can be activated into the tumor microenvironment
and results in the promotion of the IL-10+
IL-12- phenotype of TAM. Blocking IL-10, as well as other
immunosuppressive cytokines present in the tumor microenvironment, such
as TGF-
, may complement therapeutic strategies aimed at activating
type I antitumor immune responses.
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