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Our studies in immunology focus on understanding multiple aspects of the immune system and determining the molecular and cellular mechanisms of immunopathogenesis. Work from our immunology laboratories has led to novel discoveries on basic mechanisms of innate and adaptive immune regulation and on how infectious agents communicate with and influence the host immune system. These efforts have translated to therapeutic advances directed against diseases such as multiple sclerosis.

Labs in This Research Area

 Geoff Kansas Lab

T helper cell differentiation and trafficking.

Research Description

My laboratory is interested in signaling mechanisms which control T helper cell differentiation and traffic. We are currently focused on two areas: functions of p38 MAP kinases (MAPK) and the role of a transcription factor KLF2 in these processes. Toward this end, we have produced novel mouse models which will allow us to test the role of the different isoforms of p38 (of which there are 4) in T helper differentiation and expression of key leukocyte adhesion molecules; and to determine the role of KLF2 downregulation in T helper biology generally.

For lab information and more, see Dr. Kansas's faculty profile.


See Dr. Kansas's publications on PubMed.


Contact Dr. Kansas at 312-908-3237 or the lab at 312-908-3752.

 Stephen Miller Lab

Elucidation of mechanisms of pathogenesis and immune regulation of autoimmune disease, allergy and tissue/organ transplantation

Research Description

The laboratory is interested in understanding the mechanisms underlying the pathogenesis and immunoregulation of T cell-mediated autoimmune diseases, allergic disease and rejection of tissue and organ transplants.  In particular, we are studying the therapeutic use of short-term administration of costimulatory molecule agonists/antagonists and specific immune tolerance induced by infusion of antigen-coupled apoptotic cells and PLG nanoparticles for the treatment of animal models of multiple sclerosis and type 1 diabetes, allergic airway disease, as well as using tolerance for specific prevention of rejection of allogeneic and xenogeneic tissue and organ transplants.

For lab information and more, see Dr. Miller's faculty profile.


See Dr. Miller's publications on PubMed.


Contact Dr. Miller at 312-503-7674 or the lab at 312-503-1449.

Research Faculty: Andrew CogswellGabriel LorcaTobias NeefJoseph Podojil, Dan Xu

Adjunct Faculty: John Galvin

Postdoctoral Fellows: Haley Titus

Lab Manager: Sara Beddow

Technical Staff: Ming-Yi Chiang

Visiting Scholar: Michael Boyne

 Booki Min Lab

Regulatory T cells in inflammation

Research Description

The immune system is tightly controlled by multiple mechanisms, and Foxp3+ regulatory T (Treg) cells are prominent active regulators of immunity and tolerance. Defects in Treg cell generation or function result in uncontrolled systemic autoimmune inflammation. Despite extensive investigation in Treg cell biology, our understanding the mechanisms underlying Treg cell development and functions still remains incomplete. There is increasing evidence that Treg cell functions can be compromised under certain conditions, and such dysregulation is thought to be a contributing factor of chronic inflammatory conditions. Our laboratory studies both cellular and molecular factors that control Treg cell functions.

There are three major research projects currently underway in the laboratory.

1. IL-27 and Treg cells: Earlier studies had identified that IL-27, an immune regulatory cytokine produced by activated APCs, plays a non-redundant role in regulating Treg cell function. IL-27 acts on the IL-27 specific receptors (made of IL-27Ra and gp130 subunit) expressed on multiple cell types, primarily lymphocytes. Using various genetic approaches, our research focuses on identifying key source of IL-27 in autoimmune inflammation in the central nervous system and underlying mechanism by which IL-27 controls Treg cell function.

2. Glucocorticoids, miR-342, and Treg cells: We recently reported a novel role of Treg cells during glucocorticoid-induced treatment of chronic inflammation. In this study, we discovered a novel micro-RNA-342 molecule that is induced by steroid treatment in Treg cells and directly controls Treg cell metabolism. We are investigating the underlying mechanism by which this new micro-RNA-342 controls Treg cell function.

3. Lag3 and Treg cells: Lag3 is a new immune checkpoint molecule implicated in negatively regulating T cell functions. We discovered that Lag3 is induced by IL-27 stimulation in Treg cells and that Lag3 expression in Treg cells is critical for their suppressive function. We have generated several new mouse models in which Lag3 function and signaling pathways are targeted in a cell type specific manner. These novel animal models will allow us to dissect underlying mechanism of Lag3 in Treg cells and to identify potential therapeutic strategies not only to inhibit inflammation but also to enhance anti-tumor immunity by targeting Lag3 in Treg cells.

For lab information and more, see Dr. Min’s faculty profile and laboratory website.


See Dr. Min's publications.


Contact Dr. Min at 312-503-1805.

Research Faculty: Dongkyun Kim

Postdoctoral Fellows: Myung-Su Kang, Mijin Kim

Graduate Students: Giha KimRongzhen Yu

Undergraduate Student: Mia Gleason

Technical Staff: Chaimae Khaled, Sohee KimGuiqing Zhao

 Pablo Penaloza-MacMaster Lab

Immune regulation and vaccines

Research Description

How can one improve immune responses during chronic infection or cancer? How can one improve the efficacy of viral vaccines? These are 2 main questions in the Penaloza lab. A unifying concept in the lab is how innate immune responses (TLRs and IFN-I) can be harnessed to treat immune exhaustion and improve vaccines.

Recently, the Penaloza group demonstrated a potent synergy between TLR4 signaling and PD-1 blockade at reinvigorating T cell function during chronic viral infection (Wang, PLOS Pathogens, 2019). This was the first demonstration that a specific microbiome component (LPS) can potentiate immune checkpoint therapy, via a B7 costimulation dependent mechanism. The group is now investigating whether other microbial components that target innate immune receptors can also improve immune checkpoint therapy, not only against chronic infections, but also against cancer. More recently, the Penaloza laboratory developed a novel strategy to improve viral vaccines by transiently blocking IFN-I (Palacio, JEM, 2020). Although IFN-I provides a rapid antiviral protection in the setting of natural infection, IFN-I can extinguish antigen prematurely following vaccination, impinging upon the priming of adaptive immune responses. By carefully downmodulating IFN-I at the time of vaccination, his group demonstrated an improvement in vaccine efficacy, using experimental HIV-1 and coronavirus vaccines.

Dr. Penaloza’s research has also investigated the mechanisms by which T regulatory cells suppress exhausted CD8 T cells (Penaloza-MacMaster, JEM, 2014), and how lack of these suppressive mechanisms can result in lethal immunopathology following viral infection (Penaloza-MacMaster, Science, 2015).

In summary, Dr. Penaloza's research is focused on immune regulation and vaccines, with a special emphasis on understanding how innate signals and immune checkpoints regulate adaptive immunity.

For lab information and more, see Dr. Penaloza-MacMaster's faculty profile and lab website.


See Dr. Penaloza-MacMaster's publications on PubMed.


Contact Dr. Penaloza-MacMaster at 312-503-0357.

Postdoctoral Fellows: Tanushree Dangi, Kelvin (Min Han) Lew

Graduate Students: Bakare AwakoaiyeYoung Rock Chung, Nicole Palacio, Sarah Sanchez

 Chyung-Ru Wang Lab

Antigen Presentation, T-Cell Development and Regulation, Infectious Diseases and Autoimmune Diseases

Research Description

Our lab focuses on two of the MHC class Ib molecules, H2-M3 and CD1. These molecules have unusual binding specificity for antigens that are conserved in bacteria. H2-M3 presents N-formylated peptides to cytotoxic T cells while CD1 presents lipid antigens to several distinct subsets of T cells. The high degree of conservation of these microbial antigens combined with the limited polymorphism of M3 and CD1 make these two molecules attractive targets for T-cell based vaccines against intracellular pathogens for a genetically diverse population. We have generated several animal models to examine the roles of M3 and CD1 in T cell development, autoimmune diseases and defense against infectious agents, including Listeria monocytogenes and Mycobacterium tuberculosis. Using these model systems, we study the mechanisms that regulate the selection and in vivo function of M3-restricted and CD1-restricted T cells. Additionally, these models are used to characterize novel microbial antigens recognized by MHC class Ib-restricted T cells. Studies on this relatively uncharacterized segment of the mammalian immunologic repertoire may lead to improved methods for vaccination against infectious diseases.

For lab information and more, see Dr. Wang's faculty profile.


See Dr. Wang's publications on PubMed.


Contact Dr. Wang at 312-503-9748 or the lab at 312-503-1093.

Postdoctoral Fellows: Yongyong Cui, Sandeep KumarYen-Lin Lin, Manjunath Pichipally

Graduate Students: Samantha Genardi, Eva Morgun

Technical Staff: Ying He, Shon Thomas