Jin Mo Park, Ph.D.

Associate Professor of Dermatology Harvard Medical School Associate Biologist (Dermatology) Massachusetts General Hospital


Massachusetts General Hospital
Cutaneous Biology Research Center
Building 149 13th Street
Charlestown, MA 02129
Tel: (617) 643-2328
Fax: (617) 726-4453

Inflammation is a response of the immune system to microbial infection and diverse forms of tissue injury. Although inflammation per se is a protective and healing process against pathogenic stimuli, it may cause more damage than the inciting events unless its magnitude and timing are tightly controlled. Hence, insufficient inflammatory responses often lead to susceptibility to infection while excessive responses results in chronic inflammatory diseases. Our research interest is mainly focused on the inflammatory responses regulated by the IKK/NF-κB and MAPK signaling pathways. We aim at identifying regulatory targets of these signaling pathways and understanding their function in initiation, progression and resolution of inflammation.

Specific aims of the research

Function of IKK and MAPK signaling pathways in cutaneous inflammation
The objective of this part of research is to delineate the sequence of events that are responsible for skin inflammatory response. We wish to understand the role of IKK/NF-kB and MAP kinase signaling in the inflammatory responses of keratinocytes, dermal fibroblasts and skin-resident inflammatory cells. In addition, we will determine whether the inflammatory responses in the skin can be blocked by inhibiting the pro-inflammatory signaling modules and/or their regulatory targets. These studies will provide a molecular framework for the prevention and treatment of skin inflammatory diseases and secondary pathologic conditions that they incur.

Mechanism of immune recognition and induction of defense response
Macrophages and T cells play central roles in resisting microbial infection. They orchestrate the immune response by recognizing pathogen-associated molecular patterns (PAMPs) and specific antigens, respectively, and producing cytokines in order to alert the remainder of the immune system to the presence of the pathogens. We try to understand how immune receptors and multiple signaling modules are wired into a biochemical circuitry that supports stimulus-specific immune responses in macrophages and T cells. Control motifs found in the immune signaling network will offer insight into mechanisms of coordinated regulation of immune effector functions.


View my recent publications at PubMed

1.  Park JM, Greten FR, Li ZW, and Karin M. Macrophage apoptosis by anthrax lethal factor through p38 MAP kinase inhibition. Science 2002; 297:2048-2051.

2.  Hsu L-C, Park JM, Zhang K, Luo J-L, Maeda S, Kaufman RJ, Eckmann L, Guiney DG, and Karin M. The protein kinase PKR is required for macrophage apoptosis after activation of Toll-like receptor 4. Nature 2004; 428:341-345.

3.  Park JM, Brady H, Ruocco MG, Sun H, Williams D, Lee SJ, Kato Jr T, Richards N, Chan K, Mercurio F, Karin M, and Wasserman SA. Targeting of Tak by the NF-kB protein Relish regulates the JNK-mediated immune response in Drosophila. Genes Dev. 2004; 18:584-594.

4.  Park JM, Ng VH, Rest RF, and Karin M. Anthrolysin O and other Gram-positive cytolysins are Toll-like receptor 4 agonists. J. Exp. Med. 2004; 200: 1647-1655.

5.  Park JM, Greten, FR, Wong A, Westrick RJ, Arthur JSC, Otsu K, Hoffmann A, Montminy M and Karin M. Signaling pathways and genes that inhibit pathogen-induced macrophage apoptosis - CREB and NF-kB as key regulators. Immunity 2005; 23: 319-329.

6. Mahieu T, Park JM, Revets H, Pasche B, Lengeling A, Staelens J, Wullaert A, Vanlaere I, Hochepied T, van Roy F, Karin M, and Libert C. The wild-derived inbred mouse strain SPRET/Ei is resistant to LPS and defective in IFN-b production. Proc. Natl. Acad. Sci. USA 2006; 103: 2292-2297. *Equal contribution.

7.  Guichard A, Park JM, Cruz-Moreno B, Karin M, and Bier E. Anthrax lethal factor and edema factor act on conserved targets in Drosophila. Proc. Natl. Acad. Sci. USA 2006; 103: 3244-3249.

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