Fathman Lab In the Division of Immunology & Rheumatology

Fathman Lab Alumni

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Swati Acharya, PhD

Current Position: Basic Life Science Research Associate, Department of Pediatrics, Stanford University School of Medicine

Education:

Postdoctoral: Stanford University School of Medicine, Palo Alto, CA
Graduate: Tufts University School of Medicine, Boston, MA (PhD-Genetics)
Arizona State University, Tempe, AZ (M.S- Microbiology)
Andhra University, AP, India (M.S. – Applied Microbiology)
Undergraduate: Andhra University, AP, India (B.S. Chemistry)

Project: Tregs and Teffectors

Email:


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Rahima Akter

Current Position: Research Associate 3, Bristol-Myers Squibb

Education:

Postdoctoral: Stanford University
Graduate: M.Sc. in Experimental Medicine, McGill University, Montreal, Canada
M.Sc. Biophysics Institute, Federal University of Rio de Janeir
Undergraduate: M.B.B.S (Bachelor of Medicine and Bachelor of Surgery), Bangladesh

Project: Role of DEAF-1 in the pathogenesis of Type-1 Diabetes Mellitus, and the role of GRAIL E3 ligase in the regulation of T-cell tolerance

Email:


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Pearl Chang

Position: Medical Student

Education:

Undergraduate: Stanford University, Class of 2004


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Guangyu Chen, PhD

Position: Visiting Research Associate

Education:

Postdoctoral: Beijing Institute of Basic Medical Sciences, Beijing, China
Graduate: Beijing Institute of Pharmacology and Toxicology, Beijing, China
Undergraduate: B.S., Shandong University, Jinan, China

Project: Identification and characterization of CD86/CD80 binding partner in T effector cells and its biological mechanism in the suppressive immune response mediated by CTLA-4 / CD86 or CD80 pathway.


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Remi J Creusot, PhD

Current Position: Assistant Professor of Medical Sciences, Columbia University Medical Center

Education:

Postdoctoral: Stanford University
Graduate: PhD Immunology, University College London, UK
Undergraduate: BS Biochemistry, MS Microbiology & Enzymology, University of Nancy, France

Project: Pathogenesis of type I diabetes in the non-obese diabetic mouse model: mechanisms of peripheral tolerance that maintain insulitis into a non-invasive form and their failure during the transition from non-invasive to invasive/destructive insulitis; role of Deaf1 and stromal cells in enforcing peripheral tolerance; role of microRNAs in the pathogenesis of the disease. Cellular gene therapy of type I diabetes using dendritic cells modified by lentiviral transduction or mRNA electroporation to express immunoregulatory cytokines.


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Hongwu Du, PhD

Position: Visiting Research Associate

Education:

Postdoctoral: School of Medicine, Tsinghua University, Beijing, China
Graduate: Chinese Academy of Medical Sciences and Peking Union Medical College (CAMS&PUMC), Beijing, China
Undergraduate: Shandong University, Jinan, China

Project: I am attempting to set up a baseline immune profile of normal tissue samples at the single-cell level from PBCs harvested from normal individuals at different ages. It is important to know which immune system gene(s) change their expression with age. Using state of the art immune monitoring technology, and a step-by-step research protocol, it should be possible to define changes in immune profile as a function of age. This data set would serve as an important control for future studies of gene expression in disease states of older people.


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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

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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Diana Gómez-Martín, MD, PhD

Position: Postdoctoral Scholar

Education:

Postgraduate: Stanford University
Graduate: MD, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico city, Mexico.
MSc Immunology, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico city, Mexico.
PhD Immunology, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico city, Mexico.
Undergraduate: Brown University, B.S. Biology

Project: GRAIL and Autoimmunity: Identification of novel GRAIL substrates and their role in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus. Evaluation of GRAIL and endosomal trafficking of substrates. Characterization of GRAIL epistatic regulators (i.e. otubain 1 and USP8) interaction and their role in T cell responsiveness.


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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:
    1. Analysis of the effect and mechanism of action of soluble CD83 as therapy for a mouse model of inflammatory arthritis
    2. Analysis of the mechanism of action of anti-CD3 antibody in NOD mice treatment
    3. Analysis of MCC (Mutated in Colorectal Cancer Gene) function
    4. Treatment of NOD mice with GRAIL transduced Tcells

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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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Keiichi Kodama, MD/PhD

Position: Assistant Professor - Institute for Computational Health Sciences, Department of Pediatrics, University of California, San Francisco

Education:

Residency: Keio University, School of Medicine
Medical: Gunma University, M.D., Faculty of Medicine
Graduate: Keio University, Ph.D., School of Medicine

Project: Road Map Study

Email: keiichi.kodama@ucsf.edu
Lab website: http://kodamalab.ucsf.edu/
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Jack Lin, PhD

Position: Postdoctoral Scholar

Education:

Graduate: Dartmouth Medical School, Ph.D. Microbiology & Immunology
Undergraduate: Brown University, B.S. Biology

Project:

    1. The intersection of anergy genes and mTOR signaling in directing T cell activation and differentiation
    2. Examining the mechanism of action of mTOR-targeting small molecule therapeutics and validation via RNA interference
    3. Functional characterization of anergy-associated genes and their role in T cell activation and T cell lymphoma/leukemia
    4. Utilizing novel genome-wide expression profile microarray screens on human lymphocytes and human lymphomas/leukemias to identify new targets for immunotherapy

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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.

Neil's Papers from PubMed


Guo Luo, PhD

Current Position: Postdoctoral Research Fellow, Department of Psychiatry and Behavioral Sciences, Stanford University, CA

Education:

Postdoctoral: Stanford University, CA
Graduate: Doctor of Philosophy, Peking University, China (2013) Undergraduate: Bachelor of Engineering, Xi'An Jiaotong University, China (2004)

Email:


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Teppei Matsumura, PhD

Position: Postdoctoral Scholar

Education:

Graduate: Ph.D., Medicine, Osaka University, Japan M.S., Biology, Kobe University, Japan
Undergraduate: B. Sc., Kobe University, Japan

Project: Understanding the mechanism of alternative splicing of Deaf1 in pancreatic lymph nodes of NOD mice, and identification and characterization of Deaf1binding partner in pancreatic lymph node and its biological mechanisms

Email:


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Claudia Sandoval Montes, Ph.D.

Position: Postdoctoral Scholar

Education:

Postdoctoral: Dept. Molecular Biomedicine, CINVESTAV-IPN, México City, Mexico, Ph.D. Molecular Biomedicine
Graduate: Dept. Molecular Biomedicine, CINVESTAV-IPN, México City, Mexico, M.Sc. Molecular Biomedicine
Undergraduate: Universidad Nacional Autónoma de México (UNAM), México City, México, B.Sc. Pharmacological and Biological Chemistry

Project :Understanding why CD4 tumor infiltrating lymphocytes (TILs) are unresponsive is the focus of my work. Have they been rendered anergic or have they been rendered unresponsive by Tregs? If the mechanism of CD4 TIL unresponsiveness can be characterized, there may be targets of opportunity for drug development. The ubiquitin E3 ligase, GRAIL, is involved in the induction and maintenance of anergy and regulation in CD4 T cells. I plan to characterize GRAIL, its epistatic regulators, Otubain-1 and USP8, and their interactions in generating and maintaining anergic/non-responsive CD4 TILs.


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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).

Home Page: http://www.linkedin.com/in/evinoloprofile


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Chan Whiting, PhD

Position: Staff Scientist

Education:

Postdoctoral: Stanford University; Tularik/Amgen
Graduate: University of California, Los Angeles, CA
Undergraduate: University of California, Los Angeles, CA

Project: Understand the molecular basis of autoimmunity with emphasis on investigating the role of GRAIL E3 ligase in regulation of T cell tolerance/nonresponsiveness Investigate the molecular mechanisms of effective immune therapies against type 1 diabetes (T1D) and other autoimmune disorders Apply ‘omics (genomic and proteomic) approaches to identifying and understanding the functions of key regulators and targets of autoimmunity

Email:

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