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BIDMC Research Investigator / Faculty Information

Guo-Min Deng MD,PhD

Rheumatology

Contact Information:

 
Title:   Instructor
Office:   CLS-0928A
Phone:   6177354167
Fax:   6177354170
Email:   gdeng@bidmc.harvard.edu
Address:   Beth Israel Deaconess Medical Center
 330 Brookline Ave; CLS-0928A
 Boston, MA 02215

Advanced Degree And Training Info:

Year

Institution

Area or Rank

2001  Gothenburg University Sweden  Immunology
2002  National Institutes of Health (NIH) Bethesda MD  IRTA fellow
2003  National Institutes of Health (NIH) Bethesda MD  PRAT fellow
2006  Harvard Medical School Boston MA  Instructor

Research Team Listing

Lena Liu

Areas of Interest:

Immunology, Transplantation

Infectious Diseases, Inflammation   

Major Research Theme:

1. The role of lipid rafts in the pathogenesis of systemic lupus erythematosus (SLE).  In lupus-prone MRL/lpr mice, we found that lipid raft clustering forms on surface of T cells and disrupted or accelerated lripid raft clustering delays or promoted lupus pathology progression. Our studies demonstrate that lipid rafts make an important contribution in the pathogenesis of SLE (Deng GM, et al. J Immunology, 2008). We are further determining the mechanism whereby lipid rafts regulate lupus pathology progression.

2. Functions of TNF receptor PLAD.  PLAD has been found to exert a crucial role in TNFR signaling pathway.  We have made recombinant PLAD protein and discovered that PLAD protein of TNFR1 and TNFR2 blocks effect of TNFa and TNFR1 PLAD inhibits inflammatory arthritis (Deng GM, et al. Nature Medicine, 2005). To further understand the function of TNFR PLAD, we are investigating the role of TNFR PLAD in the pathogenesis of SLE.

3. Pathogenesis and therapy of cutaneous lupus erythematosus.  Skin disease is the second most common manifestation in patients with SLE.  Skin injury also exists in the lupus-prone MRL/lpr mice.  We have recently observed that signaling through tumor necrosis factor (TNF) receptor 1 is involved in the expression of skin injury in the lupus-prone mice. We are investigating how cutaneous lesions develop in SLE and whether inhibitor of TNFR1 inhibits skin injury in lupus-prone MRL/lpr mice.

Select Major Publications:    List of Publications via PubMed database at NIH NLM

Deng GM, Nilsson IM, Verdrengh M, Collins LV, Tarkowski A.Intra-articularly localized bacterial DNA containing CpG motifs induces arthritis. Nat Med. 1999 Jun;5(6):702-5.
Deng GM, Verdrengh M, Liu ZQ, Tarkowski A.The major role of macrophages and their product tumor necrosis factor alpha in the induction of arthritis triggered by bacterial DNA containing CpG motifs. Arthritis Rheum. 2000 Oct;43(10):2283-9.
Deng GM, Liu ZQ, Tarkowski A.Intracisternally localized bacterial DNA containing CpG motifs induces meningitis.  J Immunol. 2001 Oct 15;167(8):4616-26.
Deng GM, Zheng L, Chan FK, Lenardo M.Amelioration of inflammatory arthritis by targeting the pre-ligand assembly domain of tumor necrosis factor receptors. Nat Med. 2005 Oct;11(10):1066-72.
Deng GM, Tsokos GC. Cholera Toxin B Accelerates Disease Progression in Lupus-Prone Mice by Promoting Lipid Raft Aggregation  J Immunol. 2008 181: 4019-4026.

External Recognition:

PRAT fellowship (2003-2006), NIGMS, NIH.
Junior faculty travel award (AAI).  2007.

Investigator's Web Site:

        

Harvard Catalyst Site:

   
 

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