Justin Kline, MD


  • Assistant Professor, Department of Medicine, Section of Hematology/Oncology, Comprehensive Cancer Center, Committee on Immunology, Committee on Cancer Biology


B.S., Illinois Benedictine College
M.D., University of Chicago


The University of Chicago
KCBD 6128
900 East 57th Street
Chicago, Illinois 60637


Phone: (773) 702-5550


While it is now well recognized that the immune system can detect tumor antigens, spontaneous tumor rejection is rare due to the activation of immunosuppressive mechanisms within the tumor microenvironment. In alignment with this, several of the more promising cancer immunotherapies stem from the depletion of regulatory cells or blockade of coinhibitory molecules. In solid malignancies, a large number of immune escape pathways have been identified. On the other hand, immunoregulatory pathways which modulate immune responses against hematological malignancies, such as acute myeloid leukemia (AML), have been less well explored, and are a primary focus of investigation in our laboratory. Recently, we have discovered that leukemia antigen-specific T cells are deleted in a model of murine AML and that deletional tolerance can be reversed upon host APC activation (Zhang et al. 2013). Ongoing research in our laboratory involves the following projects:

Identification of the antigen presenting cell (APC) mediating tolerance to murine AML

We hypothesize that deletion of tumor specific T cells in AML bearing hosts could be due to antigen presentation by immature APC or by antigen presentation by a specific APC subset. While, several classes of APC have been shown to cross-present dying cells, latex beads, or tumor cells growing in a solid mass, the APC population that cross-presents leukemia antigens to CD8+ T cells is unknown and its identification is a major goal of the lab. Recent data from our lab suggest that the CD8a DC subset appears to be uniquely capable of engulfing AML cells in vivo and of cross-presenting leukemia-derived antigens to T cells in vitro.  In ongoing studies, we are utilizing genetic mouse models to facilitate the study of anti-leukemia T cell responses in the presence of absence of specific populations of potentially tolerogenic APC.

Strategies to reverse tolerance in hosts with established AML

Because T cell tolerance in hosts with AML appears to occur at the level of the cross-presenting APC, another goal of the laboratory is to identify strategies which target the activation/maturation of APC, such as agonistic CD40 ligation, systemic administration of toll-like receptor agonists, and engineering AML cells to express the immunogenic calreticulin protein.  We expect that following activation of “tolerogenic” host APC, effective leukemia-specific T cell responses will be generated.  Several of these concepts have potential translational application as immunotherapeutics for human AML, which is also a goal in our lab.

Generation of genetic murine AML models

To date, much of what has been learned about the anti-tumor immune response has come from studies with transplantable tumor cell lines.  While there are many advantages to the use of well-established cell lines, one important caveat is that they do not accurately recapitulate many aspects of the development and progression of human cancer.  Therefore, another major focus of our laboratory over the past two years has been to develop mouse models of AML which involve oncogenes commonly activated in human AML.  The ultimate goal of this project is to have at hand an autochthonous AML model in which immune surveillance and evasion can be investigated.

Lab members

Xiufen Chen Ph.D. - Postdoctoral Scholar
Emily Curran, M.D. – Postdoctoral Fellow
Dominick Fosco - Technician
Doug Kline - Graduate Student
Liping Meng, Ph.D. - Postdoctoral Scholar

Research Papers in PubMed