Booki  Min,  D.V.M., Ph.D.

Booki Min, D.V.M., Ph.D.

Staff

Lerner Research Institute, 9500 Euclid Avenue, Cleveland, Ohio 44195
Location: NB3-77
Email: minb@ccf.org
Phone: (216) 445-3126

 


T lymphocytes (T cells) are the main immune cells that play a central role in protecting us from pathogens. However, T cell responses must be tightly controlled, because uncontrolled responses often result in inflammatory diseases in human. One key mechanism that regulate immune responses is a subset of T cells known as regulatory T cell (Treg). Treg are essential component of the immune system. Treg suppress immune responses, diminishing inflammation. Defects in Treg generation or function result in systemic autoimmune diseases in human and mouse leading to premature death. Therefore, understanding Treg biology is an important subject of investigation. In my laboratory, we investigate factors that regulate Treg function. If Treg functions are too strong, then immune system is overly suppressed. On the other hand, if Treg functions are too weak, then the immune system is overly activated.

There is accumulating evidence that chronic inflammatory disorders such as autoimmune diseases and asthma are manifested by dysregulated Treg functions. Using mouse model of chronic inflammation models, we examine both cellular and molecular mechanisms by which Treg functions can be modulated. In particular, we use: Experimental Autoimmune Encephalomyelitis, a mouse model for human Multiple Sclerosis; T cell-induced colitis, a mouse model for human Inflammatory Bowel Disease; and allergic airway inflammation, a mouse model for human asthma. Our ongoing studies have identified that a soluble immune mediator called “Interleukin-27” is essential for Treg to properly regulate inflammation. Using a newly developed genetically engineered mouse model in which the receptor for “Interleukin-27” is selectively missing only on Treg, we found that these animals are highly susceptible to every inflammatory models tested. Furthermore, if Treg are pre-stimulated with “Interleukin-27”, they become highly potent suppressor cells. This is especially exciting because Treg infusion therapy is currently being implemented in treating chronic inflammatory diseases in human.

In other words ...

  • Roles of regulatory T cells in chronic inflammatory diseases


DongKyun  Kim  PhD DongKyun Kim, PhD
Postdoctoral Research Fellow
Location:NB3-48
Phone:(216) 445-3083
kimd3@ccf.org
Sohee  Kim  Sohee Kim
Research Technologist
Location:NB3-48
Phone:(216) 445-3083
kims2@ccf.org
Thi Hong Nga  Le  PhD Thi Hong Nga Le, PhD
Postdoctoral Research Fellow
Location:NB3-48
Phone:(216) 445-3803
let4@ccf.org
Juyeun  Lee  DVM/PHD Juyeun Lee, DVM/PHD
Postdoctoral Fellow
Location:NB3-48
Phone:(216) 445-3083
leej30@ccf.org
Quang Tam  Nguyen  PhD Quang Tam Nguyen, PhD
Postdoctoral Research Fellow
Location:NB3-48
Phone:(216) 445-3803
nguyenq@ccf.org

D. Kim, H.T. Le, Q.T. Nguyen, S. Kim, J. Lee, and B. Min. (2019). Cutting Edge: IL-27 attenuates autoimmune neuroinflammation via Treg/Lag3-dependent but IL-10-independent mechanisms in vivo. J.Immunol. In Press.

Q. T. Nguyen, E. Jang, H. T. Le, S. Kim, D. Kim, N. Dvorina, M. A. Aronica, W. M. Baldwin III, K. Asosingh, S. Comhair, and B. Min. (2019). IL-27 targets Foxp3+ Tregs to mediate anti-inflammatory functions during experimental allergic airway inflammation. JCI Insight. In Press.

Spontaneous T cell proliferation: A physiologic process to create and maintain homeostatic balance and diversity of the immune system. (2018). Front. Immunol. 9:547.

Jang ENguyen QTKim SKim DLe THNKeslar KDvorina NAronica MA Min B (2018). Lung infiltrating Foxp3+regulatory T cells are quantitatively and qualitatively different during eosinophilic and neutrophilic allergic airway inflammation but essential to control the inflammation. J. Immunol. 199:3943-3951.

Treg specific IL-27Ra deletion uncovers a key role for IL-27 in Treg function to control autoimmunity. (2017). Proc. Natl. Acad. Sci. USA. 114:10190-10195.

Heterogeneity and stability in Foxp3+ regulatory T cells. J. Interferon Cytokine Res. (2017). Epub ahead of print.

An IL-27/LAG3 axis enhances Foxp3+ regulatory T cell suppressive function and therapeutic efficacy. (2016). Mucosal Immunol. 9:137-145.

IL-27, targeting antigen presenting cells, enhances Th17 differentiation and inflammation by upregulating Th17 promoting cytokine production. (2014). Mucosal Immunol. 7:625-633.

Memory CD4 T cells induce selective expression of IL-27 in CD8+ DC and regulate homeostatic naïve T cell proliferation. (2012). J. Immunol. 188:230-237.

Cutting Edge: Basophils are transiently recruited to the draining lymph node during helminth infection via IL-3 but infection-induced Th2 immunity develops without basophil LN recruitment or IL-3. (2010). J. Immunol. 184: 1143-1147.

Differential requirements of MHC and of DCs for endogenous proliferation of different T-cell subsets in vivo. Proc. Natl. Acad. Sci. USA (2009). 106: 20394-20398.


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