The David H. Koch Institute for Integrative Cancer Research at MITThe David H. Koch Institute for Integrative Cancer Research at MIT

Massachusetts Institute of Technology

National Cancer Institute Cancer Center

Science + Engineering... Conquering Cancer Together

Stefani Spranger, PhD

Howard S. (1953) and Linda B. Stern Career Development Professor

Assistant Professor of Biology

Member, Ludwig Center at MIT


KI Research Areas of Focus:
Cancer ImmunologyPersonalized Medicine


“Our laboratory is interested in understanding the mechanisms underlying interactions between cancer and the immune system. In studying mouse models designed to mimic tumor progression in humans, our primary goal is to explain the co-evolution of the anti-tumor immune response and cancer. Knowing the interplay between tumor and immune cells will help to develop and improve effective immunotherapies against cancer.”

Stefani Spranger is an Assistant Professor of Biology at MIT. She received her bachelor's and master's degrees from the Ludwig-Maximilians University in Munich. She received her PhD in 2011 from the Helmholtz-Zentrum Munich, Institute for Molecular Immunology, where she conducted her doctoral work under the supervision of Professor Dolores J. Schendel. Professor Spranger completed her postdoctoral training at the University of Chicago in the laboratory of Professor Thomas F. Gajewski. During this period, she was supported by a German Research Foundation postdoctoral fellowship and subsequently received the Cancer Research Institute's Irvington Postdoctoral Fellowship. Spranger currently is a Scholar of the William Guy Forbeck Research Foundation, holds the Howard S. and Linda B. Stern Career Development Professorship, and is a Pew-Stewart Scholar for Cancer Research. Professor Spranger is a member of the Scientific Advisory Board of Arcus Biosciences, Replimune, Tango, and Venn Therapeutics. In addition, she acts as advisor to Dragonfly, Merck, Ribon, Takeda, and Torque Therapeutics.

Research Summary

Professor Spranger studies the interactions between cancer and the immune system, with the goal of improving existing immunotherapies or developing novel therapeutic approaches. Over the last decade, cancer immunotherapies have revolutionized cancer treatment, but despite recent advances, only a fraction of cancer patients respond to immunotherapeutic interventions. The presence of CD8 T cells, otherwise known as cytolytic, "killer" T cells, within the tumor microenvironment is known to be a key factor in response to checkpoint blockade therapy. Professor Spranger aims to understand what factors contribute to T cell exclusion from the tumor microenvironment, including tumor cell-intrinsic, tissue-macroenvironmental or environmental factors (e.g. infections). The lab focuses on lung cancer and pancreatic cancer, which serve respectively as models of immunotherapy sensitive and resistant cancer types. 

For more information about Professor Spranger’s research, please visit the Spranger lab webpage.

Selected Publications

Horton B, Spranger S. A Tumor Cell-Intrinsic Yin-Yang Determining Immune Evasion. Immunity. 2018 Jul 17;49(1):11-13. doi: 10.1016/j.immuni.2018.07.001.

Fessenden TB, Duong E, Spranger S. A team effort: natural killer cells on the first leg of the tumor immunity relay race. J Immunother Cancer. 2018 Jul 9;6(1):67. doi: 10.1186/s40425-018-0380-4.

Spranger S, Dai D, Horton B, Gajewski TF. 2017. Tumor-Residing Batf3 Dendritic Cells Are Required for Effector T Cell Trafficking and Adoptive T Cell Therapy. Cancer Cell 31: 711–723.e4.

Spranger S, Luke JJ, Bao R, Zha Y, Hernandez KM, Li Y, Gajewski AP, Andrade J, Gajewski TF. 2016. Density of immunogenic antigens does not explain the presence or absence of the T-cell-inflamed tumor microenvironment in melanoma. Proc Natl Acad Sci USA 113: E7759–E7768.

Spranger S, Bao R, Gajewski TF. 2015. Melanoma-intrinsic β-catenin signalling prevents anti-tumour immunity. Nature 523: 231–235.

Spranger S, Koblish HK, Horton B, Scherle PA, Newton R, Gajewski TF. 2014. Mechanism of tumor rejection with doublets of CTLA-4, PD-1/PD-L1, or IDO blockade involves restored IL-2 production and proliferation of CD8(+) T cells directly within the tumor microenvironment. J Immunother Cancer 2: 3.

Spranger S, Spaapen RM, Zha Y, Williams J, Meng Y, Ha TT, Gajewski TF. 2013. Up-regulation of PD-L1, IDO, and T(regs) in the melanoma tumor microenvironment is driven by CD8(+) T cells. Sci Transl Med 5: 200ra116.

Spranger S, Frankenberger B, Schendel DJ. 2012. NOD/scid IL-2Rg(null) mice: a preclinical model system to evaluate human dendritic cell-based vaccine strategies in vivo. J Transl Med 10: 30.

Spranger S, Jeremias I, Wilde S, Leisegang M, Stärck L, Mosetter B, Uckert W, Heemskerk MHM, Schendel DJ, Frankenberger B. 2012. TCR-transgenic lymphocytes specific for HMMR/Rhamm limit tumor outgrowth in vivo. Blood 119: 3440–3449.

Spranger S, Javorovic M, Bürdek M, Wilde S, Mosetter B, Tippmer S, Bigalke I, Geiger C, Schendel DJ, Frankenberger B. 2010. Generation of Th1-polarizing dendritic cells using the TLR7/8 agonist CL075. J Immunol 185: 738–747.

Search PubMed for Spranger lab Publications

Articles and Media

Learn more about Stefani Spranger's approach to cancer immunotherapy.  Or read why a new lab can be a valuable destination for postdocs and graduate students.

Listen to Stefani Spranger discussing "Deciphering Immuno-Oncology: Targeting innate immunity in cancer."


Contact Information

Stefani Spranger

room 76-453D
phone (617) 715-5882

Spranger Lab


Administrative Assistant:

Paul Thompson
phone (617) 258-0480