Charles E. Egwuagu, Ph.D.

Senior Investigator

Molecular Immunology Section

NEI

Building 10, Room 10N248G,10 Center Drive,Bethesda,MD-20892

301-496-0049

EgwuaguC@nei.nih.gov

Research Topics

The Molecular Immunology Section (MIS) seeks an integrated understanding of molecular and cellular mechanisms that regulate host immunity. Particular emphasis is on: (i) mechanisms that regulate lymphocyte development and cell-fate decisions; (ii) identifying and characterizing lymphocyte subsets that mediate or suppress CNS (central nervous system) autoimmune diseases; (iii) developing biologics and cell-based therapies for CNS inflammatory diseases, such as uveitis, multiple sclerosis and age-related macular degeneration (AMD). Use of genetically altered mouse strains and cell types has led to our discovery of novel Regulatory B cell (Breg) populations that suppress inflammation through production of the immune-suppressive cytokines, Interleukin 27 (i27-Breg) or IL-35 (i35-Breg). The long-term goal of our research program is to develop i27-Breg and i35-Breg immunotherapies for the treatment of CNS autoimmune and neurodegenerative diseases and also chronic graft-versus-host disease (GVHD).

Biography

Dr. Charles E. Egwuagu is an Epidemiologist/Immunologist and Chief of the Molecular Immunology Section, National Eye Institute. He received his Ph.D. and M.Phil. from Yale University and an M.P.H from the Yale School of Medicine, New Haven, Connecticut. Dr. Egwuagu then served as a Commissioned Officer of the USA Public Health Service, attaining the rank of Captain (06). Major research focus in the Egwuagu laboratory is on autoreactive lymphocytes that mediate CNS autoimmune diseases, such as Uveitis and Multiple Sclerosis. Particular interest is on cytokine signaling and epigenetic mechanisms that regulate lymphocyte development and cell-fate decisions. The ultimate goal is to develop Biologics and autologous regulatory B cell (Breg) immunotherapy for autoimmune and neurodegenerative diseases.

Selected Publications

  1. Amadi-Obi A, Yu CR, Liu X, Mahdi RM, Clarke GL, Nussenblatt RB, Gery I, Lee YS, Egwuagu CE. TH17 cells contribute to uveitis and scleritis and are expanded by IL-2 and inhibited by IL-27/STAT1. Nat Med. 2007;13(6):711-8.

  2. Egwuagu CE, Yu CR. Interleukin 35-Producing B Cells (i35-Breg): A New Mediator of Regulatory B-Cell Functions in CNS Autoimmune Diseases. Crit Rev Immunol. 2015;35(1):49-57.

  3. He C, Yu CR, Sun L, Mahdi RM, Larkin J 3rd, Egwuagu CE. Topical administration of a suppressor of cytokine signaling-1 (SOCS1) mimetic peptide inhibits ocular inflammation and mitigates ocular pathology during mouse uveitis. J Autoimmun. 2015;62:31-8.

  4. Dambuza IM, He C, Choi JK, Yu CR, Wang R, Mattapallil MJ, Wingfield PT, Caspi RR, Egwuagu CE. IL-12p35 induces expansion of IL-10 and IL-35-expressing regulatory B cells and ameliorates autoimmune disease. Nat Commun. 2017;8(1):719.

  5. Wang RX, Yu CR, Dambuza IM, Mahdi RM, Dolinska MB, Sergeev YV, Wingfield PT, Kim SH, Egwuagu CE. Interleukin-35 induces regulatory B cells that suppress autoimmune disease. Nat Med. 2014;20(6):633-41.


This page was last updated on February 3rd, 2020