Abstract
<div>Abstract<p>We assessed the contribution of IL1 signaling molecules to malignant tumor growth using IL1β<sup>−/−</sup>, IL1α<sup>−/−</sup>, and IL1R1<sup>−/−</sup> mice. Tumors grew progressively in IL1R<sup>−/−</sup> and IL1α<sup>−/−</sup> mice but were often absent in IL1β<sup>−/−</sup> mice. This was observed whether tumors were implanted intradermally or injected intravenously and was true across multiple distinct tumor lineages. Antibodies to IL1β prevented tumor growth in wild-type (WT) mice but not in IL1R1<sup>−/−</sup> or IL1α<sup>−/−</sup> mice. Antibodies to IL1α promoted tumor growth in IL1β<sup>−/−</sup> mice and reversed the tumor-suppressive effect of anti-IL1β in WT mice. Depletion of CD8<sup>+</sup> T cells and blockade of lymphocyte mobilization abrogated the IL1β<sup>−/−</sup> tumor suppressive effect, as did crossing IL1β<sup>−/−</sup> mice to SCID or Rag1<sup>−/−</sup> mice. Finally, blockade of IL1β synergized with blockade of PD-1 to inhibit tumor growth in WT mice. These results suggest that IL1β promotes tumor growth, whereas IL1α inhibits tumor growth by enhancing T-cell–mediated antitumor immunity.</p></div>
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