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Leveraging the Immune System during Chemotherapy: Moving Calreticulin to the Cell Surface Converts Apoptotic Death from "Silent" to Immunogenic

¹ INSERM, U848, F-94805 Villejuif, France; ² Institut Gustave Roussy, F-94805 Villejuif, France; ³ Faculté Paris Sud-Université Paris 11, F-94805 Villejuif, France; and ⁴ INSERM, U805, Institut Gustave Roussy, F-94805 Villejuif, France

Requests for reprints: Guido Kroemer, INSERM Unit U848 "Apoptosis, Cancer & Immunity", Institut Gustave Roussy, PR1, 39 rue Camille Desmoulins, F-94805 Villejuif, France. Phone: 33-4211-6046; Fax: 33-4211-6047; E-mail: kroemer{at}igr.fr or Laurence Zitvogel, U805 and CIC BT507 INSERM, Institut Gustave Roussy, 39 rue Camille Desmoulins, F-94805 Villejuif, France. Phone: 33-4211-5041; Fax: 33-4211-6094; E-mail: zitvogel{at}igr.fr.

In contrast to prior belief, tumor cell apoptosis is not necessarily silent but can be immunogenic. By tracing how anthracyclines and -irradiation trigger immunogenic cell deaths, we found that they were causally connected to the exposure of calreticulin on the tumor cell surface, before apoptosis in the tumor cell itself occurred. Furthermore, we showed that calreticulin exposure was necessary and sufficient to increase proimmunogenic killing by other chemotherapies. Our findings suggest that calreticulin could serve as a biomarker to predict therapy-associated immune responses, and that tactics to expose calreticulin might improve the clinical efficacy of many cancer therapies. [Cancer Res 2007;67(17):7941–4]

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