CHARLES GARRISON FATHMAN

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Deaf1 isoforms control the expression of genes encoding peripheral tissue antigens in the pancreatic lymph nodes during type 1 diabetes
    Linda Yip
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California, USA
    Nat Immunol 10:1026-33. 2009
  2. pmc Dengue-2 structural proteins associate with human proteins to produce a coagulation and innate immune response biased interactome
    Brenda B Folly
    Federal University of Parana, Pharmaceutical Sciences Post graduation Program, Av Pref Lothário Meissner 632, CEP 80210 170, Curitiba PR, Brazil
    BMC Infect Dis 11:34. 2011
  3. ncbi An array of possibilities for the study of autoimmunity
    C Garrison Fathman
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 435:605-11. 2005
  4. ncbi Molecular mechanisms of CD4+ T-cell anergy
    C Garrison Fathman
    Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, CCSR Building, 269 Campus Drive, Room 2225, Stanford, California 94305 5166, USA
    Nat Rev Immunol 7:599-609. 2007
  5. pmc Scratching the (T cell) surface
    Joerg Ermann
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    Genome Biol 5:202. 2003
  6. doi The transmembrane E3 ligase GRAIL ubiquitinates and degrades CD83 on CD4 T cells
    Leon L Su
    Department of Medicine, Stanford University, CA 94040, USA
    J Immunol 183:438-44. 2009
  7. ncbi Targeted gene therapy of autoimmune diseases: advances and prospects
    Remi J Creusot
    Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, CCSR Building, Room 2240, 269 Campus Drive, Stanford, CA 94305 5166, USA
    Expert Rev Clin Immunol 1:385-404. 2005
  8. ncbi Cd4+Cd25+ regulatory T cells and their therapeutic potential
    David A Randolph
    Department of Pediatrics, Division of Neonatology, Stanford University School of Medicine, Stanford, California 94305, USA
    Annu Rev Med 57:381-402. 2006
  9. pmc A model for harmonizing flow cytometry in clinical trials
    Holden T Maecker
    Institute for Immunity, Transplantation and Infection, Stanford University, Stanford, California, USA
    Nat Immunol 11:975-8. 2010
  10. pmc Naive CD4 t cell proliferation is controlled by mammalian target of rapamycin regulation of GRAIL expression
    Jack T Lin
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 182:5919-28. 2009

Research Grants

Collaborators

Detail Information

Publications37

  1. pmc Deaf1 isoforms control the expression of genes encoding peripheral tissue antigens in the pancreatic lymph nodes during type 1 diabetes
    Linda Yip
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California, USA
    Nat Immunol 10:1026-33. 2009
    ..Lower PTA expression resulting from the alternative splicing of DEAF1 may contribute to the pathogenesis of type 1 diabetes...
  2. pmc Dengue-2 structural proteins associate with human proteins to produce a coagulation and innate immune response biased interactome
    Brenda B Folly
    Federal University of Parana, Pharmaceutical Sciences Post graduation Program, Av Pref Lothário Meissner 632, CEP 80210 170, Curitiba PR, Brazil
    BMC Infect Dis 11:34. 2011
    ..We reasoned that a detailed knowledge of the global biological processes affected by virus entry into a cell might help shed new light on this long-standing problem...
  3. ncbi An array of possibilities for the study of autoimmunity
    C Garrison Fathman
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nature 435:605-11. 2005
    ..Genomic and proteomic technologies are already providing useful information about autoimmune disease, and they are likely to lead to important discoveries within the next decade...
  4. ncbi Molecular mechanisms of CD4+ T-cell anergy
    C Garrison Fathman
    Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, CCSR Building, 269 Campus Drive, Room 2225, Stanford, California 94305 5166, USA
    Nat Rev Immunol 7:599-609. 2007
    ..Controlling anergy induction and maintenance will be a key component in the future to mitigate unwanted T-cell activation that leads to autoimmune disease...
  5. pmc Scratching the (T cell) surface
    Joerg Ermann
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    Genome Biol 5:202. 2003
    ..Using a genome-scale approach to study transcription levels in a human CD8+ T-cell clone, a recent study has suggested that the repertoire of molecules on the surface of T cells is close to being completely characterized...
  6. doi The transmembrane E3 ligase GRAIL ubiquitinates and degrades CD83 on CD4 T cells
    Leon L Su
    Department of Medicine, Stanford University, CA 94040, USA
    J Immunol 183:438-44. 2009
    ..This study supports the novel mechanism of ubiquitination by GRAIL, identifies CD83 as a substrate of GRAIL, and ascribes a role for CD83 in CD4 T cell activation...
  7. ncbi Targeted gene therapy of autoimmune diseases: advances and prospects
    Remi J Creusot
    Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, CCSR Building, Room 2240, 269 Campus Drive, Stanford, CA 94305 5166, USA
    Expert Rev Clin Immunol 1:385-404. 2005
    ..This article reviews recent advances in strategies to use gene therapy in the treatment of autoimmune diseases...
  8. ncbi Cd4+Cd25+ regulatory T cells and their therapeutic potential
    David A Randolph
    Department of Pediatrics, Division of Neonatology, Stanford University School of Medicine, Stanford, California 94305, USA
    Annu Rev Med 57:381-402. 2006
    ..This article reviews what is currently known about these so-called regulatory T cells and discusses the therapeutic potential of these cells to modulate human immune-based diseases...
  9. pmc A model for harmonizing flow cytometry in clinical trials
    Holden T Maecker
    Institute for Immunity, Transplantation and Infection, Stanford University, Stanford, California, USA
    Nat Immunol 11:975-8. 2010
    ..The novel use of a central laboratory may help mitigate these issues...
  10. pmc Naive CD4 t cell proliferation is controlled by mammalian target of rapamycin regulation of GRAIL expression
    Jack T Lin
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 182:5919-28. 2009
    ..Our findings also extend the role of GRAIL beyond anergy induction and maintenance, suggesting that endogenous GRAIL regulates general cell cycle and proliferation of primary naive CD4 T cells...
  11. ncbi Only the CD62L+ subpopulation of CD4+CD25+ regulatory T cells protects from lethal acute GVHD
    Joerg Ermann
    Division of Immunology and Rheumatology, The Department of Medicine, Stanford University School of Medicine, CCSR Bldg, Rm 2215 C, 300 Pasteur Dr, Stanford, CA 94305 5166, USA
    Blood 105:2220-6. 2005
    ..The ability of Treg cells to efficiently enter the priming sites of pathogenic allo-reactive T cells appears to be a prerequisite for their protective function in aGVHD...
  12. ncbi CD4+CD25+ regulatory T cells preserve graft-versus-tumor activity while inhibiting graft-versus-host disease after bone marrow transplantation
    Matthias Edinger
    Division of Bone Marrow Transplantation, Department of Medicine, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA
    Nat Med 9:1144-50. 2003
    ..Thus, CD4+CD25+ T cells are potent regulatory cells that can separate GVHD from GVT activity mediated by conventional donor T cells...
  13. pmc L-selectin and beta7 integrin on donor CD4 T cells are required for the early migration to host mesenteric lymph nodes and acute colitis of graft-versus-host disease
    Suparna Dutt
    Department of Medicine, Stanford University School of Medicine, CCSR Building, Room 2215 C, Pasteur Drive, Stanford, CA 94305 5166, USA
    Blood 106:4009-15. 2005
    ..In conclusion, the combination of CD62L and beta7 integrin is required to induce acute colitis and facilitate entry of CD4+ donor T cells in the mesenteric nodes associated with lethal GVHD in allogeneic hosts...
  14. ncbi Murine CD4+CD25+ regulatory T cells fail to undergo chromatin remodeling across the proximal promoter region of the IL-2 gene
    Leon Su
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University, CA 94305, USA
    J Immunol 173:4994-5001. 2004
    ....
  15. ncbi Immunomodulatory vaccination in autoimmune disease
    Irene Urbanek-Ruiz
    Department of Medicine, Division of Immunology, Center for Clinical Immunology at Stanford, Stanford University School of Medicine, 269 Campus Drive, Rm 2240, Stanford, CA 94305, USA
    Endocrinol Metab Clin North Am 31:441-56, viii-ix. 2002
    ....
  16. pmc Donor-type CD4(+)CD25(+) regulatory T cells suppress lethal acute graft-versus-host disease after allogeneic bone marrow transplantation
    Petra Hoffmann
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, CA 94305, USA
    J Exp Med 196:389-99. 2002
    ..Our results demonstrate that the balance of donor-type CD4(+)CD25(+) T(reg) and conventional CD4(+)CD25(-) T cells can determine the outcome of aGVHD...
  17. ncbi The gene related to anergy in lymphocytes, an E3 ubiquitin ligase, is necessary for anergy induction in CD4 T cells
    Christine M Seroogy
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 173:79-85. 2004
    ..These data provide direct evidence that a biochemical pathway composed of GRAIL and/or GRAIL-interacting proteins is important in the development of the CD4 T cell anergic phenotype in vivo...
  18. ncbi Two isoforms of otubain 1 regulate T cell anergy via GRAIL
    Luis Soares
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305, USA
    Nat Immunol 5:45-54. 2004
    ..Thus, these two proteins have opposing epistatic functions in controlling the stability of GRAIL expression and the resultant anergy phenotype in T cells...
  19. ncbi GRAIL: an E3 ubiquitin ligase that inhibits cytokine gene transcription is expressed in anergic CD4+ T cells
    Niroshana Anandasabapathy
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, CA 94305, USA
    Immunity 18:535-47. 2003
    ..Expression of GRAIL after an anergizing stimulus may result in ubiquitin-mediated regulation of proteins essential for mitogenic cytokine expression, thus positioning GRAIL as a key player in the induction of the anergic phenotype...
  20. ncbi The subpopulation of CD4+CD25+ splenocytes that delays adoptive transfer of diabetes expresses L-selectin and high levels of CCR7
    Veronika Szanya
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, CA 94305, USA
    J Immunol 169:2461-5. 2002
    ....
  21. pmc The single subunit transmembrane E3 ligase gene related to anergy in lymphocytes (GRAIL) captures and then ubiquitinates transmembrane proteins across the cell membrane
    Neil Lineberry
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305, USA
    J Biol Chem 283:28497-505. 2008
    ..These findings identify for the first time a single subunit E3 ligase containing a substrate-binding domain spatially restricted by a membrane from its E2 recruitment domain as well as an E3 ligase for members of the tetraspanin family...
  22. ncbi Naive and memory T cells induce different types of graft-versus-host disease
    Suparna Dutt
    Department of Medicine, Stanford University School of Medicine, CA 94305, USA
    J Immunol 179:6547-54. 2007
    ..Nevertheless, the expected increase in potency as compared with naive T cells was not observed due to differences in the pattern and kinetics of tissue injury...
  23. pmc Gene therapy for type 1 diabetes: a novel approach for targeted treatment of autoimmunity
    Remi J Creusot
    Department of Medicine, Division of Immunology and Rhematology, Stanford University School of Medicine, Stanford, Califormia 94305, USA
    J Clin Invest 114:892-4. 2004
    ..This method contrasts with other targeted therapies that attempt to modify peripheral tolerance, which is also defective in type 1 diabetes mellitus...
  24. ncbi A novel E3 ubiquitin ligase substrate screen identifies Rho guanine dissociation inhibitor as a substrate of gene related to anergy in lymphocytes
    Leon Su
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford, CA 94305, USA
    J Immunol 177:7559-66. 2006
    ..These findings validate our prokaryotic screen as a method of identifying substrates for ubiquitin E3 ligases and suggest a role for Rho effector molecules in T cell anergy...
  25. ncbi T cell anergy: where it's LAT
    Neil Lineberry
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305, USA
    Immunity 24:501-3. 2006
    ..T cell receptor engagement activates selective signaling pathways in T lymphocytes under different conditions. In this issue of Immunity, demonstrate that anergic T cells are selectively defective in LAT activation...
  26. pmc Tissue- and age-specific changes in gene expression during disease induction and progression in NOD mice
    Keiichi Kodama
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, 269 West Campus Drive, Stanford, CA 94305, USA
    Clin Immunol 129:195-201. 2008
    ..These studies identified tissue- and age-specific changes in gene expression that may play an important role in the inductive or destructive events of T1D...
  27. ncbi Treatment of autoimmune disease by adoptive cellular gene therapy
    Ingo H Tarner
    Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305, USA
    Ann N Y Acad Sci 998:512-9. 2003
    ....
  28. pmc Cutting edge: The transmembrane E3 ligase GRAIL ubiquitinates the costimulatory molecule CD40 ligand during the induction of T cell anergy
    Neil B Lineberry
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 181:1622-6. 2008
    ..These data provide a model for intrinsic T cell regulation of costimulatory molecules and a molecular framework for the initiation of clonal T cell anergy...
  29. pmc Tissue-targeted therapy of autoimmune diabetes using dendritic cells transduced to express IL-4 in NOD mice
    Remi J Creusot
    Department of Medicine, Division of Immunology and Rheumatology, Stanford, CA 94305 5166, USA
    Clin Immunol 127:176-87. 2008
    ....
  30. ncbi Adoptive cellular gene therapy of autoimmune disease
    Anthony J Slavin
    Stanford University School of Medicine, Department of Medicine, Division of Immunology and Rheumatology, Stanford University, Stanford University Medical Center, 300 Pasteur Dve, CCSR 2225, Stanford, CA 94305, USA
    Autoimmun Rev 1:213-9. 2002
    ....
  31. ncbi The potential for gene therapy in the treatment of autoimmune disease
    Ingo H Tarner
    Department of Rheumatology, Stanford University School of Medicine, California 94305 5166, USA
    Clin Immunol 104:204-16. 2002
  32. ncbi Essential role of the E3 ubiquitin ligase Cbl-b in T cell anergy induction
    Myung Shin Jeon
    Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, California 92121, USA
    Immunity 21:167-77. 2004
    ..Our results show a critical role for Cbl-b in the regulation of peripheral tolerance and anergy of T cells...
  33. ncbi T-cell anergy: from phenotype to genotype and back
    Christine M Seroogy
    Department of Pediatrics, University of Wisconsin, Madison, WI, USA
    Immunol Res 28:255-64. 2003
    ....
  34. pmc The CD8alpha(+) dendritic cell is responsible for inducing peripheral self-tolerance to tissue-associated antigens
    Gabrielle T Belz
    Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Victoria 3050, Australia
    J Exp Med 196:1099-104. 2002
    ....
  35. ncbi GRAIL is up-regulated in CD4+ CD25+ T regulatory cells and is sufficient for conversion of T cells to a regulatory phenotype
    Debra A MacKenzie
    Department of Pediatrics, Division of Allergy Immunology Rheumatology, University of Wisconsin, Madison, Wisconsin 53792, USA
    J Biol Chem 282:9696-702. 2007
    ..These data demonstrate that GRAIL is differentially expressed in naturally occurring and peripherally induced CD25(+) T regulatory cells and that the expression of GRAIL is linked to their functional regulatory activity...
  36. ncbi Does our current understanding of the molecular basis of immune tolerance predict new therapies for autoimmune disease?
    Ingo H Tarner
    Department of Internal Medicine and Rheumatology, Justus Liebig University of Giessen, Kerckhoff Klinik Bad Nauheim, Division of Rheumatology and Clinical Immunology, Bad Nauheim, Germany
    Nat Clin Pract Rheumatol 2:491-9. 2006
    ..These landmarks of immune-tolerance research are summarized and their potential use in the immunotherapy of autoimmune disease discussed...
  37. pmc High cell surface expression of CD4 allows distinction of CD4(+)CD25(+) antigen-specific effector T cells from CD4(+)CD25(+) regulatory T cells in murine experimental autoimmune encephalomyelitis
    Jinzhu Li
    Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, Michigan 48201, United States
    J Neuroimmunol 192:57-67. 2007
    ..These cells displayed characteristics of Treg, such as expressing high levels of the Foxp3 gene and the ability to suppress mitogenic T cell responses...

Research Grants42

  1. Strategies for Prevention of Autoimmunity
    C Fathman; Fiscal Year: 2005
    ..If any of these strategies are successful, it is planned to progress to clinical trial application under future funding from this program. ..
  2. CD25+ Regulator CD4+ T Cells
    C Fathman; Fiscal Year: 2005
    ..More recent findings have suggested a role for GRAIL expression in peptide-induced tolerance in vivo in mice. ..
  3. International Congress of Immunology - Travel Awards
    C Fathman; Fiscal Year: 2004
    ..Twenty % of our Congress Faculty are women and 10% are either members of visible minorities or come from the homelands of US and Canadian minorities. ..
  4. Novel Anergy Genes as Markers of Immune Tolerance
    C Fathman; Fiscal Year: 2003
    ..More recent findings have suggested a role for GRAIL expression in peptide-induced tolerance in vivo in mice. Three specific aims are proposed to examine this hypothesis. ..
  5. TERNARY COMPLEX THAT DRIVES T CELL ACTIVATION
    C Fathman; Fiscal Year: 2003
    ..Utilizing recently developed techniques of retroviral-mediated transduction of murine T cells should allow functional analysis of the new genes described above found in states of T cell anergy. ..
  6. Adoptive Cellular Gene Therapy in Type 1 Diabetes (T1D)
    C Fathman; Fiscal Year: 2006
    ..Finally, under requested R33 support, a Phase I trial of transduction and infusion of autologous DCs into recently hyperglycemic T1D patients for safety studies and to observe cell trafficking is proposed. ..
  7. Deaf1 isoforms control changes in PTA expression in the NOD PLN during T1D pathog
    CHARLES GARRISON FATHMAN; Fiscal Year: 2010
    ..The studies proposed here will examine the role of Deaf1 in maintaining peripheral tolerance and help us understand how a change in Deaf1 splicing may contribute to the pathogenesis of T1D. ..
  8. Immunoregulation of Autoimmunity
    CHARLES FATHMAN; Fiscal Year: 2007
    ..abstract_text> ..
  9. Training Program in Adult and Pediatric Rheumatology
    CHARLES FATHMAN; Fiscal Year: 2007
    ..D. and Jim Fries M.D. will serve as co-PIs. The ultimate goal of this training program is the development of outstanding physician-scientists in the area of basic or clinical investigations in immunology and rheumatology. ..
  10. TERNARY COMPLEX THAT DRIVES T CELL ACTIVATION
    C Fathman; Fiscal Year: 2007
    ..If this proves correct, it will open studies of an exciting pathway of cellular signaling whose dysregulation has important implications in cancer and autoimmunity. ..
  11. FOCIS New Investigator Travel Awards (2004-2008)
    C Fathman; Fiscal Year: 2006
    ..At the third annual FOCIS meeting, 36% of the meeting attendees were woman, 25% were new investigators, and 25% were minority. ..
  12. FOCIS Annual Meetings (2002-2006)
    C Fathman; Fiscal Year: 2002
    ..By sharing discoveries with one another, delegates acquire new ideas for research and applied science from disciplines to which they would otherwise not be exposed at disease- or organ-specific meetings. ..
  13. IMMUNOTHERAPY IN DIABETES--THE NONOBESE DIABETIC MOUSE
    C Fathman; Fiscal Year: 2001
    ..It is proposed that such studies may provide an understanding of components of the pathophysiology of human IDDM. ..
  14. IMMUNOTHERAPY IN MURINE DIABETES; THE NOD MOUSE
    C Fathman; Fiscal Year: 1993
    ....
  15. IMMUNOTHERAPY IN DIABETES
    C Fathman; Fiscal Year: 1990
    ..5 and 13.4 to be used in these studies, for the production of immunotoxins using commercially available diptheria toxin, as well as the technology for islet transplantation...