Charles E Egwuagu

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Interleukin 35: Critical regulator of immunity and lymphocyte-mediated diseases
    Charles E Egwuagu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute NEI, National Institutes of Health NIH, Bethesda, MD 20892, USA Electronic address
    Cytokine Growth Factor Rev 26:587-93. 2015
  2. ncbi request reprint Ocular Inflammatory Diseases: Molecular Pathogenesis and Immunotherapy
    C E Egwuagu
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Building 10, Room 10N109A, 10 Center Drive, Bethesda, MD 20892 1857, USA
    Curr Mol Med 15:517-28. 2015
  3. doi request reprint Chronic intraocular inflammation and development of retinal degenerative disease
    Charles E Egwuagu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Building 10, Room 10N116, 10 Center Drive, 20892 1857, Bethesda, MD, USA
    Adv Exp Med Biol 801:417-25. 2014
  4. ncbi request reprint Interferon-gamma induces regression of epithelial cell carcinoma: critical roles of IRF-1 and ICSBP transcription factors
    C E Egwuagu
    Laboratories of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 1857, USA
    Oncogene 25:3670-9. 2006
  5. pmc STAT3 in CD4+ T helper cell differentiation and inflammatory diseases
    Charles E Egwuagu
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, USA
    Cytokine 47:149-56. 2009
  6. ncbi request reprint SOCS5 mRNA levels in peripheral blood mononuclear cells (PBMC): a potential bio-marker for monitoring response of uveitis patients to Daclizumab therapy
    Charles E Egwuagu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 1857, USA
    J Autoimmun 24:39-46. 2005
  7. ncbi request reprint Activation of STAT signaling pathways and induction of suppressors of cytokine signaling (SOCS) proteins in mammalian lens by growth factors
    Samuel Ebong
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Invest Ophthalmol Vis Sci 45:872-8. 2004
  8. pmc Suppressor of cytokine signaling-1 (SOCS1) inhibits lymphocyte recruitment into the retina and protects SOCS1 transgenic rats and mice from ocular inflammation
    Cheng Rong Yu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Invest Ophthalmol Vis Sci 52:6978-86. 2011
  9. ncbi request reprint Suppressor of cytokine signaling 3 regulates proliferation and activation of T-helper cells
    Cheng Rong Yu
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 278:29752-9. 2003
  10. ncbi request reprint Cell proliferation and STAT6 pathways are negatively regulated in T cells by STAT1 and suppressors of cytokine signaling
    Cheng Rong Yu
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 173:737-46. 2004

Collaborators

Detail Information

Publications50

  1. pmc Interleukin 35: Critical regulator of immunity and lymphocyte-mediated diseases
    Charles E Egwuagu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute NEI, National Institutes of Health NIH, Bethesda, MD 20892, USA Electronic address
    Cytokine Growth Factor Rev 26:587-93. 2015
    ....
  2. ncbi request reprint Ocular Inflammatory Diseases: Molecular Pathogenesis and Immunotherapy
    C E Egwuagu
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Building 10, Room 10N109A, 10 Center Drive, Bethesda, MD 20892 1857, USA
    Curr Mol Med 15:517-28. 2015
    ..This review summarizes the pathophysiology of uveitis, molecular mechanisms that regulate the initiation and progression of uveitis and concludes with emerging strategies for the treatment of this group of potentially blinding diseases. ..
  3. doi request reprint Chronic intraocular inflammation and development of retinal degenerative disease
    Charles E Egwuagu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Building 10, Room 10N116, 10 Center Drive, 20892 1857, Bethesda, MD, USA
    Adv Exp Med Biol 801:417-25. 2014
    ....
  4. ncbi request reprint Interferon-gamma induces regression of epithelial cell carcinoma: critical roles of IRF-1 and ICSBP transcription factors
    C E Egwuagu
    Laboratories of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 1857, USA
    Oncogene 25:3670-9. 2006
    ....
  5. pmc STAT3 in CD4+ T helper cell differentiation and inflammatory diseases
    Charles E Egwuagu
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, USA
    Cytokine 47:149-56. 2009
    ....
  6. ncbi request reprint SOCS5 mRNA levels in peripheral blood mononuclear cells (PBMC): a potential bio-marker for monitoring response of uveitis patients to Daclizumab therapy
    Charles E Egwuagu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 1857, USA
    J Autoimmun 24:39-46. 2005
    ..Our data also suggest that SOCS5 may serve as a new therapeutic target for uveitis and other autoimmune diseases...
  7. ncbi request reprint Activation of STAT signaling pathways and induction of suppressors of cytokine signaling (SOCS) proteins in mammalian lens by growth factors
    Samuel Ebong
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Invest Ophthalmol Vis Sci 45:872-8. 2004
    ....
  8. pmc Suppressor of cytokine signaling-1 (SOCS1) inhibits lymphocyte recruitment into the retina and protects SOCS1 transgenic rats and mice from ocular inflammation
    Cheng Rong Yu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Invest Ophthalmol Vis Sci 52:6978-86. 2011
    ..The purpose of this study was to investigate the role of SOCS1 in intraocular inflammatory diseases (uveitis) and whether SOCS1 expression is defective in patients with ocular inflammatory diseases...
  9. ncbi request reprint Suppressor of cytokine signaling 3 regulates proliferation and activation of T-helper cells
    Cheng Rong Yu
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 278:29752-9. 2003
    ..Taken together, these results suggest a role for SOCS3 in maintaining T-helper cells in a quiescent state. Transient inhibition of SOCS3 by antigen stimulation may therefore be essential in allowing activation of resting T-cells...
  10. ncbi request reprint Cell proliferation and STAT6 pathways are negatively regulated in T cells by STAT1 and suppressors of cytokine signaling
    Cheng Rong Yu
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 173:737-46. 2004
    ....
  11. ncbi request reprint Pertussis toxin is superior to TLR ligands in enhancing pathogenic autoimmunity, targeted at a neo-self antigen, by triggering robust expansion of Th1 cells and their cytokine production
    Chiaki Fujimoto
    Laboratory of Immunology, National Eye Institute, National Institute of Health, Bethesda, MD 20892 1857, USA
    J Immunol 177:6896-903. 2006
    ....
  12. ncbi request reprint Inflammatory processes triggered by TCR engagement or by local cytokine expression: differences in profiles of gene expression and infiltrating cell populations
    Hiroshi Takase
    Laboratory of Immunology, National Eye Institute, NIH, Building 10, 10 Center Drive, Bethesda, MD 20892 1857, USA
    J Leukoc Biol 80:538-45. 2006
    ....
  13. ncbi request reprint Central immunotolerance in transgenic mice expressing a foreign antigen under control of the rhodopsin promoter
    Don Il Ham
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Invest Ophthalmol Vis Sci 45:857-62. 2004
    ..The present study was aimed at analyzing the state of tolerance in Tg mice expressing hen egg lysozyme (HEL) under control of the rhodopsin promoter...
  14. ncbi request reprint Dendritic cell maturation requires STAT1 and is under feedback regulation by suppressors of cytokine signaling
    Sharon H Jackson
    Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 172:2307-15. 2004
    ....
  15. ncbi request reprint The level of thymic expression of RPE65 inversely correlates with its capacity to induce experimental autoimmune uveitis (EAU) in different rodent strains
    Don Il Ham
    Laboratory of Immunology, National Eye Institute, National Institute of Health, Bethesda, MD 20892 1857, USA
    Exp Eye Res 83:897-902. 2006
    ....
  16. pmc Interleukin 27 induces the expression of complement factor H (CFH) in the retina
    Ahjoku Amadi-Obi
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD, USA
    PLoS ONE 7:e45801. 2012
    ....
  17. pmc Thymic expression of peripheral tissue antigens in humans: a remarkable variability among individuals
    Hiroshi Takase
    National Eye Institute, NIH, Building 10, Room 10N112, Bethesda, MD 20892, USA
    Int Immunol 17:1131-40. 2005
    ....
  18. ncbi request reprint Characterization of the roles of STAT1 and STAT3 signal transduction pathways in mammalian lens development
    Samuel Ebong
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 1857, USA
    Mol Vis 10:122-31. 2004
    ..Therefore, we examined whether these growth factors mediate their effects in the lens through the evolutionarily conserved JAK/STAT signal transduction pathway and if STAT signaling is essential for mammalian lens development...
  19. ncbi request reprint TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1
    Ahjoku Amadi-Obi
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Med 13:711-8. 2007
    ....
  20. pmc Suppressors of cytokine-signaling proteins induce insulin resistance in the retina and promote survival of retinal cells
    Xuebin Liu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892 1857, USA
    Diabetes 57:1651-8. 2008
    ....
  21. pmc SOCS3 deletion in T lymphocytes suppresses development of chronic ocular inflammation via upregulation of CTLA-4 and expansion of regulatory T cells
    Cheng Rong Yu
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892
    J Immunol 191:5036-43. 2013
    ..Thus, SOCS3 is a potential therapeutic target in uveitis and other autoinflammatory diseases. ..
  22. pmc Loss of STAT3 in CD4+ T cells prevents development of experimental autoimmune diseases
    Xuebin Liu
    Section of Molecular Immunology, Laboratory of Immunology, National Eye Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
    J Immunol 180:6070-6. 2008
    ....
  23. doi request reprint Persistence of IL-2 expressing Th17 cells in healthy humans and experimental autoimmune uveitis
    Cheng Rong Yu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 1857, USA
    Eur J Immunol 41:3495-505. 2011
    ..Thus, Th17 cells may persist in tissues and contribute to chronic inflammation by limiting IL-2 production to levels that cannot provoke IL-2-induced AICD yet are sufficient to promote Th17 homeostatic expansion...
  24. pmc Interleukin-35 induces regulatory B cells that suppress autoimmune disease
    Ren Xi Wang
    1 Molecular Immunology Section, Laboratory of Immunology, National Eye Institute NEI, National Institutes of Health NIH, Bethesda, Maryland, USA 2 Laboratory of Immunology, Institute of Basic Medical Sciences, Beijing, China
    Nat Med 20:633-41. 2014
    ..As IL-35 also induced the conversion of human B cells into Breg cells, these findings suggest that IL-35 may be used to induce autologous Breg and IL-35(+) Breg cells and treat autoimmune and inflammatory disease. ..
  25. ncbi request reprint Suppressors of cytokine signaling proteins are differentially expressed in Th1 and Th2 cells: implications for Th cell lineage commitment and maintenance
    Charles E Egwuagu
    Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 168:3181-7. 2002
    ....
  26. pmc STAT3 activates miR-155 in Th17 cells and acts in concert to promote experimental autoimmune uveitis
    Thelma Escobar
    Laboratory of Immunology, National Institute of Allergy and Infectious Diseases NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    Invest Ophthalmol Vis Sci 54:4017-25. 2013
    ..In our study, we used miR-155(-/-) mice and mice with targeted STAT3 deletion in T cells (CD4-STAT3KO) to investigate roles of miR-155 and STAT3 in the development of experimental autoimmune uveitis (EAU), a mouse model of human uveitis...
  27. pmc Novel IL27p28/IL12p40 cytokine suppressed experimental autoimmune uveitis by inhibiting autoreactive Th1/Th17 cells and promoting expansion of regulatory T cells
    Ren Xi Wang
    Molecular Immunology Section, Laboratory of Immunology, NEI, National Institutes of Health, Bethesda, Maryland 20892 1857, USA
    J Biol Chem 287:36012-21. 2012
    ....
  28. ncbi request reprint T cell tolerance to a neo-self antigen expressed by thymic epithelial cells: the soluble form is more effective than the membrane-bound form
    Meifen Zhang
    National Eye Institute and National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 170:3954-62. 2003
    ....
  29. pmc Autoreactive memory CD4+ T lymphocytes that mediate chronic uveitis reside in the bone marrow through STAT3-dependent mechanisms
    Hyun Mee Oh
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 187:3338-46. 2011
    ....
  30. pmc STAT3 regulates proliferation and survival of CD8+ T cells: enhances effector responses to HSV-1 infection, and inhibits IL-10+ regulatory CD8+ T cells in autoimmune uveitis
    Cheng Rong Yu
    Molecular Immunology Section, National Eye Institute, National Institutes of Allergy and Viral Diseases, National Institutes of Health, Building 10, Room 10N109A, 10 Center Drive, Bethesda, MD 20892 1857, USA
    Mediators Inflamm 2013:359674. 2013
    ....
  31. pmc Therapeutic targeting of STAT3 (signal transducers and activators of transcription 3) pathway inhibits experimental autoimmune uveitis
    Cheng Rong Yu
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 7:e29742. 2012
    ....
  32. pmc STAT3 protein interacts with Class O Forkhead transcription factors in the cytoplasm and regulates nuclear/cytoplasmic localization of FoxO1 and FoxO3a proteins in CD4(+) T cells
    Hyun Mee Oh
    Molecular Immunology Section, NEI, National Institutes of Health, Bethesda, MD 20892, USA
    J Biol Chem 287:30436-43. 2012
    ....
  33. pmc Retinal cells suppress intraocular inflammation (uveitis) through production of interleukin-27 and interleukin-10
    Yun Sang Lee
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 1857, USA
    Immunology 132:492-502. 2011
    ..Targeted delivery of IL-27 into immune privileged tissues of the CNS may therefore be beneficial in the treatment of CNS inflammatory diseases, such as uveitis and multiple sclerosis...
  34. pmc SOCS1 regulates CCR7 expression and migration of CD4+ T cells into peripheral tissues
    Cheng Rong Yu
    Laboratory of Immunology, Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 181:1190-8. 2008
    ....
  35. pmc Key role for IL-21 in experimental autoimmune uveitis
    Lu Wang
    Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 108:9542-7. 2011
    ....
  36. pmc Interferon Regulator Factor 8 (IRF8) Limits Ocular Pathology during HSV-1 Infection by Restraining the Activation and Expansion of CD8+ T Cells
    Lin Sun
    Molecular Immunology Section, National Eye Institute NEI, National Institutes of Health NIH, Bethesda, Maryland, United States of America
    PLoS ONE 11:e0155420. 2016
    ..Thus, modulating IRF8 levels in T cells can be exploited therapeutically to prevent immune-mediated ocular pathology during autoimmune and infectious diseases of the eye. ..
  37. ncbi request reprint Cytokine-induced retinal degeneration: role of suppressors of cytokine signaling (SOCS) proteins in protection of the neuroretina
    Charles E Egwuagu
    National Eye Institute, National Institutes of Health, MD, USA
    Adv Exp Med Biol 572:275-81. 2006
  38. pmc STAT3 protein promotes T-cell survival and inhibits interleukin-2 production through up-regulation of Class O Forkhead transcription factors
    Hyun Mee Oh
    Molecular Immunology Section, Laboratory of Immunology, NEI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 286:30888-97. 2011
    ....
  39. pmc Suppressor of cytokine signaling 1 (SOCS1) mitigates anterior uveitis and confers protection against ocular HSV-1 infection
    Cheng Rong Yu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Building 10, Room 10N109A, 10 Center Drive, Bethesda, MD, 20892 1857, USA
    Inflammation 38:555-65. 2015
    ....
  40. pmc Dual Function of the IRF8 Transcription Factor in Autoimmune Uveitis: Loss of IRF8 in T Cells Exacerbates Uveitis, Whereas Irf8 Deletion in the Retina Confers Protection
    Sung Hye Kim
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892 and
    J Immunol 195:1480-8. 2015
    ..These results raise a cautionary note in the context of therapeutic targeting of IRF8. ..
  41. ncbi request reprint Immunotolerance toward native alphaA-crystallin in knockout mice deficient in the functional protein
    Puwat Charukamnoetkanok
    The National Eye Institute, National Institutes of Health, Bldg 10, Rm 10N112, Bethesda, MD 20892 1857, USA
    Immunol Lett 89:259-65. 2003
    ..These data suggest that nonfunctional proteins may induce immunotolerance and protect recipients of gene therapy from immunity against the native proteins...
  42. ncbi request reprint IL-4 synergistically enhances both IL-2- and IL-12-induced IFN-gamma expression in murine NK cells
    Jay H Bream
    Laboratory of Experimental Immunology, Center for Cancer Research, National Cancer Institute, Building 560, Room 31 23, Frederick, MD 21702 1201, USA
    Blood 102:207-14. 2003
    ..These data demonstrate a role for IL-4 in enhancing IFN-gamma expression in murine NK cells that is partially dependent on Stat6 in IL-2 costimulation and completely independent of Stat6 in IL-12 costimulations...
  43. pmc SOCS1 Mimetic Peptide Suppresses Chronic Intraocular Inflammatory Disease (Uveitis)
    Chang He
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat Sen University, Guangzhou 510060, China
    Mediators Inflamm 2016:2939370. 2016
    ..Thus, SOCS1-KIR suppresses uveitis and confers neuroprotective effects and might be exploited as a noninvasive treatment for chronic uveitis...
  44. pmc Cutting Edge: IL-1 Receptor Signaling is Critical for the Development of Autoimmune Uveitis
    Chi Keung Wan
    Laboratory of Molecular Immunology and the Immunology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892 and
    J Immunol 196:543-6. 2016
    ..These findings indicate the possible utility of IL-1R-blocking agents for the treatment of ocular inflammatory diseases. ..
  45. pmc Topical administration of a suppressor of cytokine signaling-1 (SOCS1) mimetic peptide inhibits ocular inflammation and mitigates ocular pathology during mouse uveitis
    Chang He
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, USA
    J Autoimmun 62:31-8. 2015
    ....
  46. pmc Interleukin 12 (IL-12) family cytokines: Role in immune pathogenesis and treatment of CNS autoimmune disease
    Lin Sun
    Molecular Immunology Section, National Eye Institute, National Institutes of Health, USA
    Cytokine 75:249-55. 2015
    ....
  47. ncbi request reprint Central tolerance mechanisms in control of susceptibility to autoimmune uveitic disease
    Igal Gery
    Laboratory of Immunology, National Eye Institute, NIH, 10 Center Drive, Bethesda, MD 20892 1857, USA
    Int Rev Immunol 21:89-100. 2002
  48. ncbi request reprint Interleukin 35-Producing B Cells (i35-Breg): A New Mediator of Regulatory B-Cell Functions in CNS Autoimmune Diseases
    Charles E Egwuagu
    Molecular Immunology Section, Laboratory of Immunology, National Eye Institute NEI, National Institutes of Health NIH, Bethesda, Maryland 20892
    Crit Rev Immunol 35:49-57. 2015
    ..We discuss the critical roles played by i35-Bregs in regulating autoimmune diseases and the potential use of adoptive Breg therapy in CNS autoimmune diseases. ..
  49. ncbi request reprint Immunoproteasome expression in a nonimmune tissue, the ocular lens
    Shaneen Singh
    Department of Biochemistry and Molecular Biology, UMDNJ New Jersey Medical School, Newark, NJ 07101, USA
    Arch Biochem Biophys 405:147-53. 2002
    ..The presence of immuno subunits in nonimmune tissues such as lens suggests that the immunoproteasome may also have nonimmune functions, such as that in lens differentiation...