
Epigenetic Mechanisms Underlying HIV-Infection Induced Susceptibility of CD4+ T Cells to Enhanced Activation-Induced FasL Expression and Cell Death
Author(s) -
Smita Ghare,
Paula M. Chilton,
Aakarsha V Rao,
Swati JoshiBarve,
Paula Peyrani,
Andrea Reyes-Vega,
Craig J. McClain,
Kendall Bryant,
Robert L. Cook,
M. Freiberg,
Shirish Barve
Publication year - 2021
Publication title -
journal of acquired immune deficiency syndromes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.162
H-Index - 157
eISSN - 1944-7884
pISSN - 1525-4135
DOI - 10.1097/qai.0000000000002526
Subject(s) - fas ligand , chromatin immunoprecipitation , h3k4me3 , histone , biology , epigenetics , microbiology and biotechnology , jurkat cells , t cell , apoptosis , regulation of gene expression , cancer research , gene expression , immune system , programmed cell death , immunology , promoter , gene , genetics
Chronic immune activation and CD4 T cell depletion are significant pathogenic features of HIV infection. Expression of Fas ligand (FasL), a key mediator of activation-induced cell death in T cells, is elevated in people living with HIV-1 infection (PLWH). However, the epigenetic mechanisms underlying the enhanced induction of FasL expression in CD4 T lymphocytes in PLWH are not completely elucidated. Hence, the current work examined the effect of HIV infection on FasL promoter-associated histone modifications and transcriptional regulation in CD4 T lymphocytes in PLWH.