H
Hazem E. Ghoneim
Researcher at St. Jude Children's Research Hospital
Publications - 27
Citations - 2411
Hazem E. Ghoneim is an academic researcher from St. Jude Children's Research Hospital. The author has contributed to research in topics: Cytotoxic T cell & Immune system. The author has an hindex of 13, co-authored 20 publications receiving 1693 citations. Previous affiliations of Hazem E. Ghoneim include Ohio State University & Cairo University.
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Journal ArticleDOI
De Novo Epigenetic Programs Inhibit PD-1 Blockade-Mediated T Cell Rejuvenation
Hazem E. Ghoneim,Yiping Fan,Ardiana Moustaki,Hossam A. Abdelsamed,Pradyot Dash,Pranay Dogra,Robert Carter,Walid Awad,Geoff Neale,Paul G. Thomas,Ben Youngblood +10 more
TL;DR: It is reported that blocking de novo DNA methylation in activated CD8 T cells allows them to retain their effector functions despite chronic stimulation during a persistent viral infection.
Journal ArticleDOI
TOX reinforces the phenotype and longevity of exhausted T cells in chronic viral infection.
Francesca Alfei,Kristiyan Kanev,Maike Hofmann,Ming Wu,Hazem E. Ghoneim,Hazem E. Ghoneim,Patrick Roelli,Patrick Roelli,Patrick Roelli,Daniel T. Utzschneider,Madlaina von Hoesslin,Jolie G. Cullen,Yiping Fan,Vasyl Eisenberg,Dirk Wohlleber,Katja Steiger,Doron Merkler,Mauro Delorenzi,Mauro Delorenzi,Percy A. Knolle,Cyrille J. Cohen,Robert Thimme,Benjamin Youngblood,Dietmar Zehn +23 more
TL;DR: It is shown that TOX is a critical factor for the normal progression of T cell dysfunction and the maintenance of exhausted T cells during chronic infection, and provide a link between the suppression of effector function intrinsic to CD8 T cells and protection against immunopathology.
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Effector CD8 T cells dedifferentiate into long-lived memory cells
Ben Youngblood,Ben Youngblood,J. Scott Hale,Haydn T. Kissick,Eunseon Ahn,Xiaojin Xu,Andreas Wieland,Koichi Araki,Erin E. West,Hazem E. Ghoneim,Yiping Fan,Pranay Dogra,Carl W. Davis,Bogumila T. Konieczny,Rustom Antia,Xiaodong Cheng,Rafi Ahmed +16 more
TL;DR: Epic repression of naive-associated genes in effector CD8 T cells can be reversed in cells that develop into long-lived memory T cells while key effector genes remain demethylated, demonstrating thatMemory T cells arise from a subset of fate-permissive effector T cells.
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Depletion of Alveolar Macrophages during Influenza Infection Facilitates Bacterial Superinfections
TL;DR: It is concluded that resident AM depletion occurs during influenza infection, which establishes a niche for secondary pneumococcal infection by altering early cellular innate immunity in the lungs, resulting in pneumococCal outgrowth and lethal pneumonia.
Journal ArticleDOI
Developmental plasticity allows outside-in immune responses by resident memory T cells.
Raissa Fonseca,Raissa Fonseca,Lalit K. Beura,Lalit K. Beura,Clare F. Quarnstrom,Hazem E. Ghoneim,Hazem E. Ghoneim,Yiping Fan,Caitlin C. Zebley,Milcah C. Scott,Nancy J. Fares-Frederickson,Sathi Wijeyesinghe,Emily A. Thompson,Henrique Borges da Silva,Vaiva Vezys,Benjamin Youngblood,David Masopust +16 more
TL;DR: It is shown that T RM cells can reenter the circulation, and exhibit considerable plasticity, although they retain a proclivity to reestablish themselves in their tissue of origin.