Fathman Lab Alumni
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Ana Paula Galvao da Silva, PhD
Position: Postdoctoral Fellow
Education:
Postdoctoral: Stanford University School of Medicine, Stanford, CA (since 2003)
Graduate: Immunology PhD, University of Sao Paulo, Sao Paulo, Brazil
Undergraduate: Biomedical Science, Federal University of Pernambuco, Brazil
Project:The suppressive role of sCD83 in a mouse model of diabetes; phenotype and mechanism of action studies. The hypothesis being addressed in this proposal is that a soluble form of the cell surface molecule CD83 will prevent or treat ongoing type 1 diabetes (T1D) in NOD mice based upon preliminary findings as well as previous work in other models.
The role of GRAIL in the induction of anergic and regulatory CD4+ T cells in the tumor microenvironment. GRAIL (RNF128) is a type 1 transmembrane RING E3 ubiquitin ligase that localizes to the transferrin-recycling endocytic pathway. While very little expression in resting CD4+ T cells is observed, GRAIL mRNA and protein becomes upregulated in T cells exposed to antigen in the absence of appropriate costimulation or following peptide administration in a tolerazing fashion in vivo. CD4+ T cells infiltrating tumor masses seem to become tolerant to the tumor and in certain cases may differentiate into Tregs, which may block the anti-tumor immune response. In most cases the differentiation into Tregs is due to the lack of appropriate co-stimulation and due to the presence of regulatory molecules that down-regulate T cell activation. Our goal is to demonstrate that antigen specific CD4+ TILs express GRAIL and become anergic and regulatory, and by blocking GRAILs effects, tumor immunity can be restored.
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Hideyuki Iwai, MD/PhD
Position:Postdoctoral Scholar
Education:
Residency: Tokyo Medical and Dental University, Faculty of Medicine
Medical/Undergraduate: Tokyo Medical and Dental University, M.D., Faculty of Medicine
Graduate: Tokyo Medical and Dental University, Ph.D., Department of Medicine and Rheumatology
Project: I. Analysis of the effect
and mechanism of action of soluble CD83 as therapy for a mouse model
of inflammatory arthritis
II. Analysis of the mechanism of action of anti-CD3
antibody in NOD mice treatment
III. Analysis of MCC (Mutated in Colorectal Cancer
Gene) function
IV. Treatment of NOD mice with GRAIL transduced T
cells
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Yul Huh
Position: Graduate Student Researcher (M.S., Biological Sciences)
Education:
Undergraduate: Stanford University, B.S., Biological Sciences
Project: Characterization of novel anergy genes and their functionality in T cell activation and tumorigenesis.
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Neil Lineberry, PhD
Position: Post-doctoral scholar
Education:
Graduate: Stanford University, PhD in Immunology
Undergraduate: University of Virginia, BA in Biology
Project: I am interested in understanding the mechanisms of immune tolerance that prevent detrimental activation of the immune system against self. Since nearly all cellular protein expression is regulated by the ubiquitin-proteasome system, I am focusing on how the E3 ligase activity of GRAIL utilizes protein degradation to modulate T cell development, activation, and homeostasis. Potential applications of these projects include a greater understanding of the molecular pathogenesis of autoimmunity and other scenarios involving a breakdown in immune tolerance, such as graft rejection.
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Deqiao Sheng, PhD
Position: Postdoctoral fellow
Education:
Graduate: Chinese Academy of Medical Science & Peking Union Medical College, Ph.D. Molecular Biology
Undergraduate: Xiamen University, B.S. Biology
Project: RoadMap of NOD T1D
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Emilie Vinolo, PhD
Position: Postdoctoral Fellow
Education:
Graduate: Ph.D. in biochemistry from Universite Pierre et Marie Curie/Institut Pasteur, Paris (France)
Undergraduate: French engineering school E.S.P.C.I., Chemistry major
Project: From my PhD dissertation work on the NF-ΚB essential modulator (NEMO) protein, I became interested in exploring the interface between ubiquitination and signaling in the immune system. As a result, I joined the Fathman lab to focus on two projects. First, several bodies of evidence suggest a possible role for lymphocyte activation gene 3 (LAG-3) in the negative regulation of T cell activation and the induction and/or maintenance of tolerance. I am presently trying to identify proteins that interact with LAG-3 cytoplasmic domain in order to gain further insight into LAG-3 intracellular signaling and its regulation of T cell function. Second, I am utilizing a structure-function approach to refine the model in which expression of the E3 ligase GRAIL is regulated by two deubiquitinating enzymes, Otubain 1 and USP8 (see Soares L. et al. Nat. Immunol. 2004).
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Home Page: http://www.linkedin.com/in/evinoloprofile
