Maria-Luisa (Marisa) Alegre, M.D., Ph.D.


  • Professor, Department of Medicine - Section of Rheumatology, College Faculty Member
  • Committee on Immunology, Committee on Molecular Medicine/MPMM, Committee on Molecular Metabolism and Nutrition, Comprehensive Cancer Research Center


Ph.D., The University of Chicago, 1993
M.D., Université Libre de Bruxelles, 1985
B.S., Université Libre de Bruxelles, 1981


The University of Chicago 
JFK R312
924 East 57th Street 
Chicago, Illinois 60637

Phone:  (773) 834-4317


The Alegre laboratory is interested in T cell responses in settings of transplantation, autoimmunity and cancer, with an emphasis on mouse models and emerging extensions onto clinical translation.  The Alegre laboratory has contributed to the understanding of negative regulators of T cell activation such as CTLA-4 and PD-1 in homeostasis and during transplant rejection.  Additionally, we have studied the molecular signals in T cells that are required for rejecting transplanted organs.  Using mice with genetic alterations of T cell-NF-kB, we have shown that activation of NF-kB in T cells is absolutely required for acute rejection of cardiac allografts and select transplantable tumors, partially for islet allograft rejection and minimally for skin allograft rejection. With an interest toward developing selective inhibitors for therapeutic use, we have then studied the possible consequences of inhibiting T cell-NF-kB on various aspects of thymocyte development, T cell survival, activation and differentiation.

In collaboration with Anita Chong, the Alegre laboratory has investigated the impact of microbial signals on transplant outcomes.  We found that TLR ligands and bacterial infections could all prevent the induction of transplantation tolerance, whereas only infection with Listeria monocytogenes could break transplantation tolerance once it had been stably established.  Importantly, this breaking of tolerance was transient as the memory of tolerance prior to infection dominated over a memory of the rejection event. 

The fact that bacterial infections could enhance alloreactivity led us to ask if commensal bacteria, which share many microbial molecular patterns with pathogens, could also modulate alloimmunity and anti-tumor immunity.  We found that the absence of microbial colonization or a reduction in bacterial diversity resulted in prolongation of allograft survival by lowering dendritic cells’ ability to activate alloreactive T cells, whereas select bacteria potentiated anti-tumor immunity via tuning of dendritic cells. 

Our current work investigates the mechanisms of T cell tolerance in robust models of transplantation tolerance as well as the mechanisms by which the microbiota modulates alloreactivity.

View Research Papers on PubMed