CD27 signaling inhibits tumor metastasis via CD8+ T cell-independent mechanisms

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Presentation Time: 10:00 AM - 10:15 AM
Abstract ID: 5142 - B

Presenting Author:
Eswara Rao Puppala , Postdoctoral Fellow at Univ. of Maryland Greenebaum Comp. Cancer Ctr.

Abstract:

CD27 belongs to the tumor necrosis factor receptor (TNF) superfamily and acts as a co-stimulatory molecule, modulating T- and B-cell responses. CD27 stimulation enhances NK and T cell survival and effector functions, thus providing opportunities to develop therapeutic strategies. The current study aims to investigate the role of endogenous CD27 signaling in tumor growth and metastasis. Specific deletion of CD27 from CD8+ cells (CD8cre-CD27fl mice) was developed and confirmed by flow cytometric analysis, while CD27KO (global CD27 knockout, deletion of CD27 from all cell types) mice were also used in our studies. Tumor growth and metastasis studies were performed by injecting B16-F10 cells subcutaneously (right flank) or intravenously into the mice. Flow cytometry analyses revealed that CD27 was deleted explicitly from CD8+ cells without affecting CD4+ cells, B cells, and HSPC in CD8cre-CD27fl mice, and in the case of CD27KO mice, CD27 was deleted from all cell types. From the tumor metastasis studies, we found that CD27KO mice showed a significantly higher burden of metastatic tumor nests in the lungs compared to WT controls (P<0.0077). However, there is no significant difference in lung tumor nest count between CD8cre-CD27fl mice and WT controls. These results suggest that endogenous CD27 signaling inhibits tumor metastasis via CD8+ T cell-independent mechanisms, presumably through stimulating antitumor activities of other immune cell types.