The Great Escape

In the movie The Great Escape, “problem” prisoners with multiple escape attempts are put in an “escape-proof” POW camp, where they use their cleverness and specialized skills to outwit their captors. However, when it comes to escaping, even Steve McQueen doesn’t have anything on cancer cells. Although human cancers express tumor antigens recognized by the immune system, host immune responses often fail to control tumor growth. Taube et al. now explain one way in which tumor cells may adapt to escape from immune surveillance.
The researchers found a strong association between expression of the immune-inhibitory molecule B7-H1 (PD-L1) on melanocytes and immune cell infiltration into tumors in patients with different stages of melanoma. The B7-H1+ melanocytes were found directly adjacent to the immune cells, with interferon-γ detected at the melanocyte–immune cell interface. Interferon-γ, which is secreted by the immune cells, induces B7-H1 expression; thus, the tumor may adapt by causing immune cells to trigger their own inhibition. Indeed, patients with B7-H1+ metastatic melanoma had prolonged overall survival when compared with B7-H1 metastatic melanoma patients, perhaps suggesting that B7-H1 expression by the tumors is stimulated by a more successful immune response. It remains to be seen whether blocking B7-H1 in these patients will further improve survival. But it is clear that for both prisoners and tumors, adaptation is the key to escape.


Although many human cancers such as melanoma express tumor antigens recognized by T cells, host immune responses often fail to control tumor growth for as yet unexplained reasons. Here, we found a strong association between melanocyte expression of B7-H1 (PD-L1), an immune-inhibitory molecule, and the presence of tumor-infiltrating lymphocytes (TILs) in human melanocytic lesions: 98% of B7-H1+ tumors were associated with TILs compared with only 28% of B7-H1 tumors. Indeed, B7-H1+ melanocytes were almost always localized immediately adjacent to TILs. B7-H1/TIL colocalization was identified not only in melanomas but also in inflamed benign nevi, indicating that B7-H1 expression may represent a host response to tissue inflammation. Interferon-γ, a primary inducer of B7-H1 expression, was detected at the interface of B7-H1+ tumors and TILs, whereas none was found in B7-H1 tumors. Therefore, TILs may actually trigger their own inhibition by secreting cytokines that drive tumor B7-H1 expression. Consistent with this hypothesis, overall survival of patients with B7-H1+ metastatic melanoma was significantly prolonged compared with that of patients with B7-H1 metastatic melanoma. Therefore, induction of the B7-H1/PD-1 pathway may represent an adaptive immune resistance mechanism exerted by tumor cells in response to endogenous antitumor activity and may explain how melanomas escape immune destruction despite endogenous antitumor immune responses. These observations suggest that therapies that block this pathway may benefit patients with B7-H1+ tumors.

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Supplementary Material


Materials and Methods
Fig. S1. Geographic patterns of CD3+ TILs corresponding to the patterns of B7-H1 expression in cases shown in Fig. 1.
Fig. S2. Immunohistochemical characterization of cell types and architecture at the interface of B7-H1 expression and immune infiltrates in a melanoma lesion.
Fig. S3. Kinetics of B7-H1 induction by IFN-γ in cultured human melanoma cells.
Fig. S4. Comparison of B7-H1 detection in fresh and FFPE tissues using mAb 5H1.
Fig. S5. Comparison of B7-H1 detection by the mAb 5H1 versus the polyclonal antibody 4059.
Fig. S6. Comparative specificities of anti–B7-H1 mAb 5H1 and polyclonal antibody 4059 by Western blotting.
Fig. S7. B7-H1+ tumor and associated TILs sampled by laser capture microdissection.
Table S1. B7-H1 expression by melanocytes and infiltrating immune cells in 54 in situ and invasive primary melanomas does not correlate with pT or TNM stage.


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Published In

Science Translational Medicine
Volume 4 | Issue 127
March 2012

Submission history

Received: 9 January 2012
Accepted: 23 February 2012


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We thank R. Li, C. Umbricht, Y. Liu, and F. Housseau for helpful discussions, as well as J. Califano and J. Handa for their support (all Johns Hopkins University School of Medicine). Funding: This study was supported by grants from the National Cancer Institute (CA016359, CA97085, and CA85721 to L.C.), the NIH (R01DK080736 and R01DK081417 to R.A.A.), the Melanoma Research Alliance (to D.M.P., S.L.T., and L.C.), the Barney Family Foundation (to S.L.T.), the Michael Rolfe Foundation for Pancreatic Cancer Research (to R.A.A.), and the Dermatology Foundation (to J.M.T.). Author contributions: J.M.T., R.A.A., G.D.Y., S.C., D.M.P., S.L.T., and L.C. conceived and designed the experiments. J.M.T., R.A.A., G.D.Y., H.X., R.S., T.L.M., and S.C. performed the experiments. J.M.T., R.A.A., G.D.Y., T.L.M., S.C., A.P.K., D.M.P., S.L.T., and L.C. analyzed the data. J.M.T., D.M.P., S.L.T., and L.C. wrote the manuscript. Competing interests: S.L.T. is a consultant to (uncompensated) and S.L.T., J.M.T., R.A.A., and H.X. receive research support from Bristol-Myers Squibb. The 5H1 antibody (made in L.C.’s laboratory, U.S. 7,797,710 and U.S. 7,892,540) will be distributed via a standard University Material Transfer Agreements for research, which is consistent with Science Translational Medicine’s material sharing policy. The other authors declare that they have no competing interests.



Janis M. Taube* [email protected]
Department of Dermatology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Robert A. Anders
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Geoffrey D. Young
Department of Otolaryngology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Haiying Xu
Department of Dermatology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Rajni Sharma
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Tracee L. McMiller
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Shuming Chen
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Alison P. Klein
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Department of Oncology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Drew M. Pardoll
Department of Oncology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Suzanne L. Topalian* [email protected]
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Lieping Chen* [email protected]
Department of Dermatology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Department of Oncology, Johns Hopkins Medical Institutions, Baltimore, MD 21287, USA.
Department of Immunobiology, Yale University, New Haven, CT 06519, USA.


To whom correspondence should be addressed. E-mail: [email protected] (J.M.T.); [email protected] (S.L.T.); [email protected] (L.C.)

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