Pathology

Feng Lin, Ph.D.

Assistant Professor

Mailing Address:
11100 Euclid Ave
Cleveland, OH 44106

phone: (216) 368-2118
email: Feng.Lin@Case.edu

Biography
Dr. Feng Lin received his B.S. from NanKai University, China (1992). He completed his Ph.D. at Sichuan University, China, in 1997. That year he came to Case as a Research Associate in the Institute of Pathology. From 2001 until 2003, Dr. Lin was an Instructor in the Institute, and is presently holding an Assistant Professor position.

Research
The Complement system, as part of the immunity network, plays important roles in defending ourselves from pathogen invasion and maintaining body homeostasis. Complement activation products can recruit inflammatory cells, opsonize pathogens for phagocytosis and kill pathogens directly. They are also important for many immunological reactions including immune complex clearance, antibody production and T cell activation, etc. Insufficient or excess complement activation contribute to various disease states including transplant rejection, cancer, systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, myasthelia gravis and age related macular degeneration, etc. Using gene knock out mice and transgenic mice as disease models, our lab is interested in studying complement activation and regulation in disease states, thus eventually developing novel reagents to fight against those diseases. Currently the projects that are carrying out in our lab are:

    1. Synergetic inhibition of complement and T cell activation in EAE, an animal model for multiple sclerosis. The ultimate goal of this project is to explore whether different forms of recombinant complement inhibitors can be used to treat the disease that paralyzes people.
    2. Complement inhibition in Myasthenia gravis. The aim of this project is to develop complement inhibitor(s) that can be used to treat the MG patients upon disease onset.
    3. Complement activation and factor H in age related macular degeneration. The purpose of this project is to study the role of complement activation in the pathogenesis of AMD including drusen formation and neovascularization.


Publications
Heeger PS, Lalli PN, Lin F, Valujskikh A, Liu J, Muqim N, Xu Y, Medof ME. (2005). Decay-accelerating factor modulates induction of T cell immunity. J Exp Med. 201(10):1523-30.

Kaminski, HJ, Li, Z, Richmonds, C, Lin, F and M. Edward Medof (2004). Complement regulators in extraocular muscle and experimental autoimmune myasthenia gravis. Experimental Neurology 189(2): 333-342.

Lin F, D Spencer, AD. Levine,and ME Medof (2004). Decay Accelerating Factor Deficiency Increases Susceptibility to Dextran Sulfate Sodium-induced Colitis Journal of Immunology 172(6):3836-41.

Lin F, David J. Salant, Howard Myereson, B. Paul Morgan, Steven Emancipator and M. Edward Medof (2004). Respective Roles of DAF and CD59 in Circumventing Glomerular Injury in Acute Nephrotoxic Serum Nephritis Journal of Immunology 172(4):2636-2642.

Urinova S, F Lin, G Ball, K Bromek, D Uhrin, ME Medof and PN Barlow (2003). Solution structure of a functionally active component of decay accelerating factor. Proc Natl Acad Sci USA 100(8): 4718 – 4723.

Lin F, HJ. Kaminski, C Richmonds, and ME Medof (2002). Enhanced Susceptibility to Myasthenia Gravis in the Absence of Decay-Accelerating Factor Protection. J Clin Invest. 110(9):1269-74.

He Y, F Lin, P Chipman, C Bator, T S. Baker, M Shoham, RJ. Kuhn, ME Medof, MG. Rossmann (2002). Structure of echovirus 7 complexed with decay-accelerating factor, its cellular receptor Proc Natl Acad Sci USA 99 (16):10325-10329.

Urinova S, F Lin, D Uhrin, ME Medof and PN Barlow (2002). Resonance assignments of the central complement control protein module pair of human decay accelerating factor. J. of Biomolecular NMR 23 (2):167-168.

Lin F, S Emancipator, DJ Salant and EM Medof (2002). Decay-Accelerating Factor Confers Protection Against Complement-Mediated Podocyte Injury in Acute Nephrotoxic Nephritis. Lab Investigation 82 (5):563-570.

Lin F, Y Fukuaka and EM Medof (2001). Tissue Distribution of products of the mouse DAF genes-exploitation of a Daf1 knock-out mouse and site-specific monoclonal antibodies Immunology 104 (2):215-225.

Lin F, R Immormino, M Shoham and EM Medof (2001). Bulk production and functional analyses of mouse CD55's native and deglycosylated active domains. Archives of Biochemistry and Biophysics 393 (1): 67-72