Fathman Lab Members
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C. Garrison Fathman, M.D.
Dr. Fathman, Professor of Medicine and Chief of the Division of Immunology and Rheumatology at Stanford University School of Medicine, also serves as Past Chairman of the Federation of Clinical Immunology Societies (FOCIS) and Director of the Center for Clinical Immunology at Stanford (CCIS).
For more information about Dr. Fathman, visit the Lab Home Page.
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Swati Acharya, PhD
Position: Post Doctoral Fellow
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: Graft versus host disease (GVHD) is a chronic and debilitating systemic inflammatory disease characterized by inflammatory cell recruitment to the skin, gastrointestinal tract and other organs, and leads to a systemic chronic debilitating disease. Identification, characterization and potential uses of CD4+CD25+ regulatory T cells (Tregs) in the prevention of autoimmune/inflammatory diseases such as GVHD, is an important therapeutic approach. Although the etiology of GVHD is reasonably well understood, and the sequence of events underlying the course of the disease is well researched, no good approaches to therapy of this disease have been developed. By using a gene identification molecular approach, we believe that new targets of therapeutic intervention can be developed through deciphering the genetic signature of Tregs.
My project involves: (1) Identification the core set of CD4+CD25+ Treg genes by performing cDNA comparative microarray analysis of CD4+CD25+ vs CD4+CD25-T cells from the thymus and spleen of BALB/c and B6 mice at several different time points (age) to identify the shared core set of expressed Treg genes: ‘the core Treg transcriptome’, (2) Validation of the ‘core transcriptome’ genes based on in vitro loss-of-function studies using functional genomics (RNAi), (3) Investigating the in vivo loss of function of genes tested in (2) above using a model of GVHD. If these studies are successful in demonstrating a Treg core transcriptome, a similar approach can be taken with human Tregs to identify genes associated with loss of function in studies in vitro. (4) Identification of lineage specific genes that are involved in the development of T regulatory cells.
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Pearl Chang
Position: Medical Student
Education:
Undergraduate: Stanford University, Class of 2004
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Remi J Creusot, PhD
Position: Research Associate
Education:
Project: Pathogenesis of type I diabetes in the non-obese diabetic mouse model: initiation (role and specificity of T cells in the initial insulitic lesion), progression (from respectful to invasive insulitis), and role of stromal cells in the regulation of the autoimmune response. Cellular gene therapy of type I diabetes using modified dendritic cells (in vivo trafficking and mechanisms of therapy).Postdoctoral: Stanford University
Graduate: PhD Immunology, University College London, UK
Undergraduate: BS Biochemistry, MS Microbiology & Enzymology, University of Nancy, France
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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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Keiichi Kodama, MD/PhD
Position: Postdoctoral Scholar
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
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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.
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Leon Su, PhD
Position: Staff Scientist
Education:
Postdoctoral: Stanford University
Graduate: University of California, San Diego
Undergraduate: University of California, Berkeley
Project: Molecular Mechanisms of Peripheral T cell Tolerance
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Linda Yip, PhD
Position: Postdoctoral Fellow
Education:
Postdoctoral: Dept. of Surgery, University of California San Diego, USA
Graduate: Ph.D., Physiology, University of British Columbia, Canada
Undergraduate: B. Sc., Physiology, University of British Columbia, Canada
Project:
Type 1 Diabetes develops due to the lack of T cell tolerance to islet
antigens. T cells which recognize self-antigen are normally deleted
through central or peripheral tolerance mechanisms. Central tolerance
occurs in the thymus as developing T cells are exposed to self-antigens
expressed in medullary thymic epithelial cells. Peripheral tolerance
occurs when mature T cells circulate through the body and encounter
peripheral tissue antigens on various cells, including those of the
lymph nodes. My work focuses on the identification and characterization
of genes which regulate peripheral tissue antigen expression and peripheral
tolerance during the development of Type I diabetes.
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