Elizabeth D Mellins

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Research priorities in pediatric rheumatology: The Childhood Arthritis and Rheumatology Research Alliance (CARRA) consensus
    Sylvia Ota
    Department of Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Canada
    Pediatr Rheumatol Online J 6:5. 2008
  2. doi request reprint Pathogenesis of systemic juvenile idiopathic arthritis: some answers, more questions
    Elizabeth D Mellins
    Department of Pediatrics, Stanford University, 300 Pasteur Drive, Stanford, CA 94305, USA
    Nat Rev Rheumatol 7:416-26. 2011
  3. pmc Serum amyloid A induces mitogenic signals in regulatory T cells via monocyte activation
    Khoa D Nguyen
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA Electronic address
    Mol Immunol 59:172-9. 2014
  4. pmc Alternative activation in systemic juvenile idiopathic arthritis monocytes
    Claudia Macaubas
    Department of Pediatrics, Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Clin Immunol 142:362-72. 2012
  5. pmc Comparison of transduction efficiency among various lentiviruses containing GFP reporter in bone marrow hematopoietic stem cell transplantation
    Nan Wang
    Department of Pediatrics, Program in Immunology, Program in Human Gene Therapy, Stanford University School of Medicine, Stanford, CA, USA
    Exp Hematol 41:934-43. 2013
  6. pmc Serum amyloid A overrides Treg anergy via monocyte-dependent and Treg-intrinsic, SOCS3-associated pathways
    Khoa D Nguyen
    Department of Pediatrics, Immunology Program, Stanford University School of Medicine, 259 Campus Drive, Stanford, CA 94305, USA
    Blood 117:3793-8. 2011
  7. ncbi request reprint Structural factors contributing to DM susceptibility of MHC class II/peptide complexes
    Michael P Belmares
    Department of Chemistry, Stanford University, CA 94305, USA
    J Immunol 169:5109-17. 2002
  8. ncbi request reprint Selective developmental defects of cord blood antigen-presenting cell subsets
    Laura Drohan
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305 5164, USA
    Hum Immunol 65:1356-69. 2004
  9. pmc Bordetella pertussis infection of primary human monocytes alters HLA-DR expression
    Jennifer A Shumilla
    Department of Pediatrics Departments of Microbiology and Immunology and Medicine, Stanford University School of Medicine, Stanford, California, USA
    Infect Immun 72:1450-62. 2004
  10. pmc Correlation analyses of clinical and molecular findings identify candidate biological pathways in systemic juvenile idiopathic arthritis
    Xuefeng B Ling
    Program in Immunology, Department of Pediatrics, Stanford University, Stanford, CA 94305, USA
    BMC Med 10:125. 2012

Research Grants

Collaborators

Detail Information

Publications50

  1. pmc Research priorities in pediatric rheumatology: The Childhood Arthritis and Rheumatology Research Alliance (CARRA) consensus
    Sylvia Ota
    Department of Child Health Evaluative Sciences, The Hospital for Sick Children, Toronto, Canada
    Pediatr Rheumatol Online J 6:5. 2008
    ..One of the first projects undertaken by this network was to define, by consensus, research priorities for the group, and if possible a first group-sponsored clinical trial in which all members could participate...
  2. doi request reprint Pathogenesis of systemic juvenile idiopathic arthritis: some answers, more questions
    Elizabeth D Mellins
    Department of Pediatrics, Stanford University, 300 Pasteur Drive, Stanford, CA 94305, USA
    Nat Rev Rheumatol 7:416-26. 2011
    ..Despite much progress being made, many questions remain, providing fertile ground for future research...
  3. pmc Serum amyloid A induces mitogenic signals in regulatory T cells via monocyte activation
    Khoa D Nguyen
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA Electronic address
    Mol Immunol 59:172-9. 2014
    ..Collectively, these results point to a novel mechanism, by which SAA initiates a monocyte-dependent process that drives mitogenic signals in Treg. ..
  4. pmc Alternative activation in systemic juvenile idiopathic arthritis monocytes
    Claudia Macaubas
    Department of Pediatrics, Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Clin Immunol 142:362-72. 2012
    ..The persistence of some of these phenotypes during clinically inactive disease argues that this state reflects compensated inflammation...
  5. pmc Comparison of transduction efficiency among various lentiviruses containing GFP reporter in bone marrow hematopoietic stem cell transplantation
    Nan Wang
    Department of Pediatrics, Program in Immunology, Program in Human Gene Therapy, Stanford University School of Medicine, Stanford, CA, USA
    Exp Hematol 41:934-43. 2013
    ..Thus, among those compared, dual-promoter vector-based lentivirus with the EF1a promoter driving the gene of interest is optimal for murine BM-HSC transduction...
  6. pmc Serum amyloid A overrides Treg anergy via monocyte-dependent and Treg-intrinsic, SOCS3-associated pathways
    Khoa D Nguyen
    Department of Pediatrics, Immunology Program, Stanford University School of Medicine, 259 Campus Drive, Stanford, CA 94305, USA
    Blood 117:3793-8. 2011
    ..Collectively, these evidences suggest a novel anti-inflammatory role of SAA in the induction of a micro-environment that supports T(reg) expansion at sites of infection or tissue injury, likely to curb (auto)-inflammatory responses...
  7. ncbi request reprint Structural factors contributing to DM susceptibility of MHC class II/peptide complexes
    Michael P Belmares
    Department of Chemistry, Stanford University, CA 94305, USA
    J Immunol 169:5109-17. 2002
    ..Thus, the peptide repertoire displayed to CD4(+) T cells is the result of a mechanistically complicated editing process and cannot be simply predicted from the intrinsic stability of the complexes in the absence of DM...
  8. ncbi request reprint Selective developmental defects of cord blood antigen-presenting cell subsets
    Laura Drohan
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305 5164, USA
    Hum Immunol 65:1356-69. 2004
    ..APB monocytes also showed a greater LPS-induced increase in CD40 expression. Together, our data show significant, selective differences in circulating APC between neonates and adults...
  9. pmc Bordetella pertussis infection of primary human monocytes alters HLA-DR expression
    Jennifer A Shumilla
    Department of Pediatrics Departments of Microbiology and Immunology and Medicine, Stanford University School of Medicine, Stanford, California, USA
    Infect Immun 72:1450-62. 2004
    ..These data demonstrate that B. pertussis utilizes several mechanisms to modulate HLA-DR expression...
  10. pmc Correlation analyses of clinical and molecular findings identify candidate biological pathways in systemic juvenile idiopathic arthritis
    Xuefeng B Ling
    Program in Immunology, Department of Pediatrics, Stanford University, Stanford, CA 94305, USA
    BMC Med 10:125. 2012
    ....
  11. pmc I-Ag7 is subject to post-translational chaperoning by CLIP
    Cornelia H Rinderknecht
    Program in Immunology, Stanford University, Stanford, CA 94305, USA
    Int Immunol 22:705-16. 2010
    ..This finding indicates that, although other regions of Ii interact with class II, CLIP binding to the groove is likely to be a dominant event in assembly of nascent class II molecules with Ii in the ER...
  12. ncbi request reprint Point mutations in or near the antigen-binding groove of HLA-DR3 implicate class II-associated invariant chain peptide affinity as a constraint on MHC class II polymorphism
    Robert C Doebele
    Division of Immunology and Transplantation Biology, Department of Pediatrics, Center for Clinical Sciences Research, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 170:4683-92. 2003
    ..The profound phenotypes associated with some of these point mutations suggest that the need to maintain efficient CLIP release represents a constraint on naturally occurring MHC II polymorphism...
  13. pmc Distribution of circulating cells in systemic juvenile idiopathic arthritis across disease activity states
    Claudia Macaubas
    Program in Immunology, Division of Human Gene Therapy, Department of Pediatrics, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305 5164, USA
    Clin Immunol 134:206-16. 2010
    ..Overall, our findings suggest dysregulation of innate immunity in SJIA and raise the possibility that quiescence represents a state of compensated inflammation...
  14. pmc Mapping the HLA-DO/HLA-DM complex by FRET and mutagenesis
    Taejin Yoon
    Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 109:11276-81. 2012
    ..Collectively, our data define a putative binding surface and an overall orientation of the szDOv/sDM complex and have implications for the mechanism of DO inhibition of DM...
  15. ncbi request reprint Achieving stability through editing and chaperoning: regulation of MHC class II peptide binding and expression
    Robert Busch
    Division of Pediatric Immunology and Transplantation Biology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94705, USA
    Immunol Rev 207:242-60. 2005
    ..In this context, we discuss possible mechanisms by which the association of some MHC II alleles with autoimmune diseases may be linked to their low CLIP affinity...
  16. pmc An insertion mutant in DQA1*0501 restores susceptibility to HLA-DM: implications for disease associations
    Tieying Hou
    Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA 94305, USA
    J Immunol 187:2442-52. 2011
    ..Our findings elucidate the structural basis for reduced DQ2-DM interaction and have implications for mechanisms underlying disease associations of DQ2...
  17. pmc Monocytes are resistant to apoptosis in systemic juvenile idiopathic arthritis
    Shivani Srivastava
    Department of Biology, Stanford University, Stanford, CA, USA
    Clin Immunol 136:257-68. 2010
    ..Thus, SJIA monocytes are resistant to apoptosis due to alterations in both the extrinsic and intrinsic apoptosis pathways, and circulating factors associated with active SJIA may confer this phenotype...
  18. pmc Plasticity of T-cell phenotype and function: the T helper type 17 example
    Ariana Peck
    Department of Pediatrics, Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Immunology 129:147-53. 2010
    ....
  19. doi request reprint Oligoarticular and polyarticular JIA: epidemiology and pathogenesis
    Claudia Macaubas
    Department of Pediatrics, Stanford University, Stanford, CA 94305 5164, USA
    Nat Rev Rheumatol 5:616-26. 2009
    ..Within each subtype, however, common pathways seem to drive joint damage...
  20. ncbi request reprint Relationship between kinetic stability and immunogenicity of HLA-DR4/peptide complexes
    Frances C Hall
    Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA
    Eur J Immunol 32:662-70. 2002
    ..These data indicate that kinetic stability of peptide/MHC complexes in vivo is a key determinant of immunogenicity...
  21. ncbi request reprint Formation of two peptide/MHC II isomers is catalyzed differentially by HLA-DM
    Michael P Belmares
    Departments of Chemistry and Pediatrics, Stanford University, Stanford, California 94305, USA
    Biochemistry 42:838-47. 2003
    ..Intramolecular isomer interconversion does not appear to be involved. The behavior of these complexes may provide a model for peptide editing by DM in endosomes...
  22. ncbi request reprint Regulation of the class II MHC pathway in primary human monocytes by granulocyte-macrophage colony-stimulating factor
    Tara M C Hornell
    Department of Pediatrics, School of Medicine, Stanford University, CCSR Room 2120, 269 Campus Drive, Stanford, CA 94305, USA
    J Immunol 171:2374-83. 2003
    ..Thus, our data argue that the proinflammatory role of GM-CSF is mediated in part through increased expression of key molecules involved in the class II MHC pathway via induction of CIITA...
  23. pmc Masking of a cathepsin G cleavage site in vivo contributes to the proteolytic resistance of major histocompatibility complex class II molecules
    Timo Burster
    Division of Endocrinology and Diabetes, Department of Internal Medicine I, Ulm University, Ulm, Germany
    Immunology 130:436-46. 2010
    ....
  24. doi request reprint Cathepsin G: roles in antigen presentation and beyond
    Timo Burster
    Division of Endocrinology and Diabetes, Department of Internal Medicine I, Ulm University, Ulm, Germany
    Mol Immunol 47:658-65. 2010
    ..In this review, historical and recent data on CatG expression, distribution, function and involvement in disease will be summarized and discussed, with a focus on its role in antigen presentation and immune-related events...
  25. ncbi request reprint Stabilization of soluble, low-affinity HLA-DM/HLA-DR1 complexes by leucine zippers
    Robert Busch
    Department of Pediatrics, Stanford University Medical Center, Room 2120 CCSR Bldg, 269 Campus Drive, CA 94305 5164, USA
    J Immunol Methods 263:111-21. 2002
    ..Thus, fusion with artificial LZ domains can stabilize unstable protein-protein complexes for biochemical and structural studies of interactions within the complex...
  26. pmc Breaking old paradigms: Th17 cells in autoimmune arthritis
    Ariana Peck
    Department of Pediatrics, Division of Immunology and Transplantation Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Clin Immunol 132:295-304. 2009
    ....
  27. pmc Transgene expression in various organs post BM-HSC transplantation
    Nan Wang
    Department of Pediatrics, Program in Immunology, Program in Human Gene Therapy, Stanford University School of Medicine, Stanford, CA, USA Electronic address
    Stem Cell Res 12:209-21. 2014
    ..The results have implications for analysis of the outcomes of gene therapy when both therapeutic and reporter genes are introduced. The findings also have implications for understanding the development of immune molecule function. ..
  28. ncbi request reprint Host-derived CD4+ T cells attenuate stem cell-mediated transfer of autoimmune arthritis in lethally irradiated C57BL/6.g7 mice
    Narendiran Rajasekaran
    Stanford University School of Medicine, Stanford, California 94305 5164, USA
    Arthritis Rheum 65:681-92. 2013
    ..The objective of this study was to investigate the factors responsible for the attenuation of arthritis in B6.g7 recipients...
  29. pmc Human cytomegalovirus decreases constitutive transcription of MHC class II genes in mature Langerhans cells by reducing CIITA transcript levels
    Andrew W Lee
    Department of Pediatrics, Program in Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Mol Immunol 48:1160-7. 2011
    ..We suggest this represents a new mechanism of modulation of mature LC by HCMV...
  30. ncbi request reprint Human cytomegalovirus alters localization of MHC class II and dendrite morphology in mature Langerhans cells
    Andrew W Lee
    Department of Pediatrics, Division of Infectious Diseases, Stanford University School of Medicine, Stanford, CA 94305, USA
    J Immunol 177:3960-71. 2006
    ..Thus, HCMV impedes MHC class II molecule trafficking, dendritic projections, and migration of mature LC. These changes likely contribute to the reduced activation of CD4+ T cells by HCMV-infected mature LC...
  31. ncbi request reprint Cytokines elicited by T cell epitopes from a synovial autoantigen: altered peptide ligands can reduce interferon-gamma and interleukin-10 production
    Frances C Hall
    Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305, USA
    Arthritis Rheum 48:2375-85. 2003
    ..To explore the cytokine responses associated with T cell epitopes from human cartilage glycoprotein 39 (HC gp-39) and the potential for modifying cytokine secretion using altered peptide ligands (APLs)...
  32. ncbi request reprint Interaction of HLA-DR with an acidic face of HLA-DM disrupts sequence-dependent interactions with peptides
    Achal Pashine
    Department of Pediatrics, Stanford University, Stanford, California 94305, USA
    Immunity 19:183-92. 2003
    ..Peptide release from the complexes was fast and only weakly sequence dependent, arguing that DM diminishes the selectivity of the MHCII groove. Analysis of soluble DM action on soluble DR/peptide complexes corroborates this conclusion...
  33. pmc Self-antigen recognition by follicular lymphoma B-cell receptors
    Kacey L Sachen
    Department of Medicine, Division of Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Blood 120:4182-90. 2012
    ..These results suggest that antigen stimulation may provide survival signals to tumor cells and that there is a selective pressure to preserve antigen recognition as the tumor evolves...
  34. ncbi request reprint Urine peptidomics for clinical biomarker discovery
    Xuefeng B Ling
    Department of Pediatrics, Stanford University, Stanford, California, USA
    Adv Clin Chem 51:181-213. 2010
    ..This study summarizes, focusing on our experiences and perspectives, the progress in addressing these challenges to enable high-throughput urine peptidomics-based biomarker discovery...
  35. ncbi request reprint Human dendritic cell expression of HLA-DO is subset specific and regulated by maturation
    Tara M C Hornell
    Department of Pediatrics, Stanford University School of Medicine, 269 Campus Drive, Stanford, CA 94305, USA
    J Immunol 176:3536-47. 2006
    ..The range of APC types shown to express DO suggests a broader role for DO in immune function than previously appreciated...
  36. pmc Modulation of peripheral B cell tolerance by CD72 in a murine model
    Daniel Hsieh Hsin Li
    Stanford University School of Medicine, Stanford, California 94305, USA
    Arthritis Rheum 58:3192-204. 2008
    ..The goal of this study was to elucidate the role of CD72 in modulating B cell receptor (BCR)-mediated tolerogenic signaling and peripheral B cell tolerance...
  37. pmc HLA-DM and HLA-DO, key regulators of MHC-II processing and presentation
    Elizabeth D Mellins
    Department of Pediatrics, Program in Immunology, Stanford University, Stanford, CA 94305, United States
    Curr Opin Immunol 26:115-22. 2014
    ..We also highlight several areas where gaps persist in our knowledge about this pair of proteins and their molecular biology and immunobiology. ..
  38. pmc Plasma profiles in active systemic juvenile idiopathic arthritis: Biomarkers and biological implications
    Xuefeng B Ling
    Department of Pediatrics, Stanford University, Stanford, CA 94305 5164, USA
    Proteomics 10:4415-30. 2010
    ..Pathway analyses of the 15 proteins in the SJIA flare versus quiescence signature corroborate growing evidence for a key role for IL-1 at disease flare...
  39. pmc Regulatory T cells and their role in rheumatic diseases: a potential target for novel therapeutic development
    Diana Milojevic
    Department of Pediatrics, UCSF, San Francisco, CA 94143, USA
    Pediatr Rheumatol Online J 6:20. 2008
    ..We also review the literature on the role of these T cells in rheumatic diseases and discuss the potential for their use in immunotherapy...
  40. pmc DM influences the abundance of major histocompatibility complex class II alleles with low affinity for class II-associated invariant chain peptides via multiple mechanisms
    Cornelia H Rinderknecht
    Department of Pediatrics, Stanford University, Stanford, CA 94305 5164, USA
    Immunology 131:18-32. 2010
    ..Thus, multiple mechanisms, operating along the biosynthetic pathway of class II molecules, contribute to DM-mediated increases in the abundance of low-CLIP-affinity alleles...
  41. ncbi request reprint Candidate early predictors for progression to joint damage in systemic juvenile idiopathic arthritis
    Christy Sandborg
    Department of Pediatrics, Stanford University School of Medicine, University Medical Center, 300 Pasteur Drive, Stanford, CA 94305, USA
    J Rheumatol 33:2322-9. 2006
    ..To assess if joint damage at 2 years after diagnosis in patients with systemic juvenile idiopathic arthritis (SJIA) can be predicted by clinical or laboratory features assessed up to 3 or 6 months after diagnosis...
  42. ncbi request reprint Posttranslational regulation of I-Ed by affinity for CLIP
    Cornelia H Rinderknecht
    Program in Immunology, Department of Pediatrics, Stanford University, Stanford, CA 94305, USA
    J Immunol 179:5907-15. 2007
    ....
  43. pmc Chaperone activity of α B-crystallin is responsible for its incorrect assignment as an autoantigen in multiple sclerosis
    Jonathan B Rothbard
    Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford University, Stanford, CA 94305, USA
    J Immunol 186:4263-8. 2011
    ..HspB5 also precipitated Ig heavy and L chains from sera from patients with MS. These results establish that small Hsps bind Igs with high affinity and refute much of the serological data used to assign α B-crystallin as an autoantigen...
  44. pmc Precarious balance: Th17 cells in host defense
    Ariana Peck
    Department of Pediatrics, Division of Immunology and Transplantation Biology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Infect Immun 78:32-8. 2010
    ..However, because Th17 cells mediate both host defense and pathological inflammation, elucidation of mechanisms that attenuate but do not completely abolish the Th17 response may have powerful implications for therapy...
  45. ncbi request reprint Influenza A virus elevates active cathepsin B in primary murine DC
    Timo Burster
    Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305, USA
    Int Immunol 19:645-55. 2007
    ..Our findings indicate that influenza A virus affects the MHC class II antigen-processing pathway, an essential pathway for CD4(+) T cell activation...
  46. ncbi request reprint Latent cytomegalovirus down-regulates major histocompatibility complex class II expression on myeloid progenitors
    Barry Slobedman
    Center for Virus Research, Westmead Millennium Institute and University of Sydney, Westmead, Australia
    Blood 100:2867-73. 2002
    ....
  47. ncbi request reprint Labeling antigen-specific CD4(+) T cells with class II MHC oligomers
    Thomas O Cameron
    Department of Chemistry, MIT, 77 Massachusetts Avenue, Cambridge 02139, USA
    J Immunol Methods 268:51-69. 2002
    ....
  48. pmc DRB1*0401-restricted human T cell clone specific for the major proinsulin73-90 epitope expresses a down-regulatory T helper 2 phenotype
    Ivana Durinovic-Bello
    Department of Internal Medicine I, Division of Endocrinology, University of Ulm, D 89081 Ulm, Germany
    Proc Natl Acad Sci U S A 103:11683-8. 2006
    ....
  49. ncbi request reprint Complexes of two cohorts of CLIP peptides and HLA-DQ2 of the autoimmune DR3-DQ2 haplotype are poor substrates for HLA-DM
    Lars Egil Fallang
    Centre for Immune Regulation and Institute of Immunology, University of Oslo, Oslo, Norway
    J Immunol 181:5451-61. 2008
    ..We suggest that the unusual interaction of DQ2 with Ii and DM may provide a basis for the known disease associations of DQ2...

Research Grants5

  1. Training Cross-Disciplinary Researchers in Diabetes
    Elizabeth Mellins; Fiscal Year: 2007
    ..Achievement of this goal has the potential to contribute to new diagnostic and therapeutic approaches for diabetes and related conditions. ..
  2. A role for IL-1 in SJIA monocyte phenotypes: A RAPPORT ancillary study
    Elizabeth D Mellins; Fiscal Year: 2010
    ..We also hope to identify changes in monocytes during disease that predict response to Rilanocept. ..