International Immunology, Vol 10, 823-832, Copyright © 1998 by Oxford University Press
G Terres and RL Coffman
The effect of systemic administration of anti-inflammatory cytokines (IL-4
and IL-10) on the development and maintenance of an anti-tumor rejection
response in vivo was studied by following the growth patterns of P815.B7
tumors on B6D2F1 [(C57BI/6 x DBA/2)F1] mice. The anti- P815.B7 rejection
response was found to be T cell dependent, involving both CD4 and CD8
cells. IL-4 treatment resulted in a compromised rejection response; IL-10
treatment alone had little or no effect. These results demonstrate that
treatment with an anti-inflammatory cytokine can compromise an otherwise
effective anti-tumor rejection response. For the anti-inflammatory cytokine
IL-4, the immunosuppressive effects of the cytokine appear to outweigh any
possible anti-tumor activities as have been reported using tumor cells
genetically altered to produce IL-4. Relatively high systemic doses of
IL-10, in contrast, were not immunosuppressive and, when given in
combination with IL-4, countered the IL-4 suppressive effect.
Pathologically, IL-4 treatment led to splenomegaly characterized by a
marked increase in neutrophils and NK activity. The possible linkages
between neutrophils, NK activity and IL-12 are discussed.
ARTICLES
The role of IL-4 and IL-10 cytokines in controlling an anti-tumor response in vivo
Department of Immunobiology, DNAX Research Institute of Molecular and Cellular Biology, Inc., Palo Alto, CA 94304, USA.
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