L Wen

Summary

Affiliation: Yale University
Country: USA

Publications

  1. pmc In vivo evidence for the contribution of human histocompatibility leukocyte antigen (HLA)-DQ molecules to the development of diabetes
    L Wen
    Section of Endocrinology, Department of Internal Medicine, the Yale University Shool of Medicine, New Haven, CT, USA
    J Exp Med 191:97-104. 2000
  2. pmc The role of lymphocyte subsets in accelerated diabetes in nonobese diabetic-rat insulin promoter-B7-1 (NOD-RIP-B7-1) mice
    F S Wong
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Exp Med 187:1985-93. 1998
  3. pmc The regulatory role of DR4 in a spontaneous diabetes DQ8 transgenic model
    L Wen
    Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Clin Invest 107:871-80. 2001
  4. ncbi request reprint Identification of an MHC class I-restricted autoantigen in type 1 diabetes by screening an organ-specific cDNA library
    F S Wong
    Section of Immunobiology, Yale School of Medicine, 310 Cedar Street, New Haven, Connecticut 06520 8011, USA
    Nat Med 5:1026-31. 1999
  5. ncbi request reprint Targeted expression of the anti-apoptotic gene CrmA to NOD pancreatic islets protects from autoimmune diabetes
    I Millet
    Department of Internal Medicine and Immunobiology, Section of Endocrinology, Yale University School of Medicine, P O Box 208020, 333 Cedar Street, TAC S141, New Haven, CT 06520, USA
    J Autoimmun 26:7-15. 2006
  6. ncbi request reprint Gamma delta T cell help of B cells is induced by repeated parasitic infection, in the absence of other T cells
    W Pao
    Department of Biology, Yale University, New Haven, Connecticut 06520, USA
    Curr Biol 6:1317-25. 1996
  7. ncbi request reprint Type 1 diabetes-predisposing MHC alleles influence the selection of glutamic acid decarboxylase (GAD) 65-specific T cells in a transgenic model
    R S Abraham
    Department of Immunology, Mayo Clinic, Rochester, MN 55905 Department of Endocrinology, Yale University School of Medicine, New Haven, CT 06510, USA
    J Immunol 166:1370-9. 2001
  8. ncbi request reprint Pediatric autoimmune liver diseases: the molecular basis of humoral and cellular immunity
    L Wen
    Section of Endocrinology, Department of Medicine, Yale University, New Haven, CT 06520, USA
    Curr Mol Med 1:379-89. 2001
  9. ncbi request reprint How can the innate immune system influence autoimmunity in type 1 diabetes and other autoimmune disorders?
    L Wen
    Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, Mailbox 208020, 333 Cedar Street, New Haven, CT 06520, USA
    Crit Rev Immunol 25:225-50. 2005
  10. pmc Translational Mini-Review Series on B Cell-Directed Therapies: B cell-directed therapy for autoimmune diseases
    C Hu
    Department of Internal Medicine, Section of Endocrinology, Yale University School of Medicine, New Haven, CT 06520, USA
    Clin Exp Immunol 157:181-90. 2009

Collaborators

Detail Information

Publications19

  1. pmc In vivo evidence for the contribution of human histocompatibility leukocyte antigen (HLA)-DQ molecules to the development of diabetes
    L Wen
    Section of Endocrinology, Department of Internal Medicine, the Yale University Shool of Medicine, New Haven, CT, USA
    J Exp Med 191:97-104. 2000
    ..B7-1 C57BL/6 mice. Our data provide direct in vivo evidence for the diabetogenic effect of this human MHC class II molecule and a unique "humanized" animal model of spontaneous diabetes...
  2. pmc The role of lymphocyte subsets in accelerated diabetes in nonobese diabetic-rat insulin promoter-B7-1 (NOD-RIP-B7-1) mice
    F S Wong
    Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Exp Med 187:1985-93. 1998
    ..It is possible that B lymphocytes play an important role in the provision of costimulation in NOD mice which is unnecessary in the NOD-RIP-B7-1 transgenic mice...
  3. pmc The regulatory role of DR4 in a spontaneous diabetes DQ8 transgenic model
    L Wen
    Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Clin Invest 107:871-80. 2001
    ....
  4. ncbi request reprint Identification of an MHC class I-restricted autoantigen in type 1 diabetes by screening an organ-specific cDNA library
    F S Wong
    Section of Immunobiology, Yale School of Medicine, 310 Cedar Street, New Haven, Connecticut 06520 8011, USA
    Nat Med 5:1026-31. 1999
    ..This has very important implications for the potential use of insulin in preventative therapy...
  5. ncbi request reprint Targeted expression of the anti-apoptotic gene CrmA to NOD pancreatic islets protects from autoimmune diabetes
    I Millet
    Department of Internal Medicine and Immunobiology, Section of Endocrinology, Yale University School of Medicine, P O Box 208020, 333 Cedar Street, TAC S141, New Haven, CT 06520, USA
    J Autoimmun 26:7-15. 2006
    ..We conclude that anti-apoptotic genes such as CrmA might be potential candidates to enhance islet graft survival in T1DM...
  6. ncbi request reprint Gamma delta T cell help of B cells is induced by repeated parasitic infection, in the absence of other T cells
    W Pao
    Department of Biology, Yale University, New Haven, Connecticut 06520, USA
    Curr Biol 6:1317-25. 1996
    ..In particular, it has not been resolved whether gamma delta cells, independent of any other T cells, can help B cells produce immunoglobulin and form germinal centers, anatomical foci of specialized T cell-B cell collaboration...
  7. ncbi request reprint Type 1 diabetes-predisposing MHC alleles influence the selection of glutamic acid decarboxylase (GAD) 65-specific T cells in a transgenic model
    R S Abraham
    Department of Immunology, Mayo Clinic, Rochester, MN 55905 Department of Endocrinology, Yale University School of Medicine, New Haven, CT 06510, USA
    J Immunol 166:1370-9. 2001
    ..Thus, the presence of diabetes-associated genes determines whether immune tolerance is maintained to islet autoantigens, but autoreactivity in itself is not sufficient to induce diabetes...
  8. ncbi request reprint Pediatric autoimmune liver diseases: the molecular basis of humoral and cellular immunity
    L Wen
    Section of Endocrinology, Department of Medicine, Yale University, New Haven, CT 06520, USA
    Curr Mol Med 1:379-89. 2001
    ..The presence of cross-reactivity between homologous sequences, especially between HCV and cytochromes, supports the possibility that molecular mimicry plays a role in the induction of autoantibodies and autoreactive cytotoxic T cells...
  9. ncbi request reprint How can the innate immune system influence autoimmunity in type 1 diabetes and other autoimmune disorders?
    L Wen
    Section of Endocrinology, Department of Internal Medicine, Yale University School of Medicine, Mailbox 208020, 333 Cedar Street, New Haven, CT 06520, USA
    Crit Rev Immunol 25:225-50. 2005
    ..We will also explore the interaction of the innate immune system with adaptive immune responses in predisposing individuals to the development of autoimmunity...
  10. pmc Translational Mini-Review Series on B Cell-Directed Therapies: B cell-directed therapy for autoimmune diseases
    C Hu
    Department of Internal Medicine, Section of Endocrinology, Yale University School of Medicine, New Haven, CT 06520, USA
    Clin Exp Immunol 157:181-90. 2009
    ..Considerations for future development of B cell-directed therapy for autoimmune diseases have also been discussed...
  11. pmc T-cell alpha beta + and gamma delta + deficient mice display abnormal but distinct phenotypes toward a natural, widespread infection of the intestinal epithelium
    S J Roberts
    Department of Biology, Yale University, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 93:11774-9. 1996
    ..An immuno-downregulatory role during infection, and during autoimmune disease, may be a general one for gamma delta + cells...
  12. pmc Critical roles of CD30/CD30L interactions in murine autoimmune diabetes
    S Chakrabarty
    Division of Internal and Geriatric Medicine, Department of Development and Ageing, Kobe University Graduate School of Medicine, Kobe, Japan
    Clin Exp Immunol 133:318-25. 2003
    ..Furthermore, anti-CD30L mAb inhibited T cell proliferation in response to islet antigens. These results suggested that CD30/CD30L interaction plays important roles in both induction and effector phases of autoimmune diabetes in NOD mice...
  13. ncbi request reprint What can the HLA transgenic mouse tell us about autoimmune diabetes?
    F S Wong
    Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, Bristol, UK
    Diabetologia 47:1476-87. 2004
    ..HLA transgenic mice offer a way to elucidate the in vivo role of these molecules, and could help the development of targeted immunotherapy...
  14. ncbi request reprint Immunoglobulin synthesis and generalized autoimmunity in mice congenitally deficient in alpha beta(+) T cells
    L Wen
    Department of Biology, Yale University, New Haven, Connecticut 06511
    Nature 369:654-8. 1994
    ....
  15. pmc The neuronal repellent Slit inhibits leukocyte chemotaxis induced by chemotactic factors
    J Y Wu
    Department of Pediatrics, and Molecular Biology and Pharmacology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Nature 410:948-52. 2001
    ..In addition, we have uncovered an inhibitor of leukocyte chemotaxis, and propose a new therapeutic approach to treat diseases involving leukocyte migration and chemotactic factors...
  16. ncbi request reprint [Investigation of group A rotavirus infection in several cities in China and prevalence of VP7 serotype]
    S Xu
    Institute of Virology, Chinese Academy of Preventive Medicine, Beijing 100052, China
    Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi 15:77-80. 2001
    ..CONCLUSION: The results indicated that rotavirus was the most important etiologic agent in this country, and the predominant serotypes were G1, G2 and G3...
  17. ncbi request reprint [cDNA cloning, sequencing and expression of recombinant human prorelaxin]
    C Ding
    National Laboratory of Molecular Virology and Genetic Engineering, Beijing
    Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi 11:319-21. 1997
    ..The SDS-PAGE analysis revealed that the expressed protein accounted for about 30% of the total cell protein, its MW was approximately 20 kD and conformed soluble protein...
  18. ncbi request reprint Murine lupus in the absence of alpha beta T cells
    S L Peng
    Department of Biology, Yale University, New Haven, CT 06510, USA
    J Immunol 156:4041-9. 1996
    ....
  19. pmc Lymphocyte proliferation in mice congenitally deficient in T-cell receptor alpha beta + cells
    J L Viney
    Imperial Cancer Research Fund, London, United Kingdom
    Proc Natl Acad Sci U S A 91:11948-52. 1994
    ....