Loss of PBAF promotes expansion and effector differentiation of CD8+ T cells during chronic viral infection and cancer. Cell Rep 2023 Jun 27;42(6):112649
Date
06/18/2023Pubmed ID
37330910Pubmed Central ID
PMC10592487DOI
10.1016/j.celrep.2023.112649Scopus ID
2-s2.0-85162227177 (requires institutional sign-in at Scopus site) 18 CitationsAbstract
During chronic viral infection and cancer, it has been established that a subset of progenitor CD8+ T cells continuously gives rise to terminally exhausted cells and cytotoxic effector cells. Although multiple transcriptional programs governing the bifurcated differentiation trajectories have been previously studied, little is known about the chromatin structure changes regulating CD8+ T cell-fate decision. In this study, we demonstrate that the chromatin remodeling complex PBAF restrains expansion and promotes exhaustion of CD8+ T cells during chronic viral infection and cancer. Mechanistically, transcriptomic and epigenomic analyses reveal the role of PBAF in maintaining chromatin accessibility of multiple genetic pathways and transcriptional programs to restrain proliferation and promote T cell exhaustion. Harnessing this knowledge, we demonstrate that perturbation of PBAF complex constrained exhaustion and promoted expansion of tumor-specific CD8+ T cells resulting in antitumor immunity in a preclinical melanoma model, implicating PBAF as an attractive target for cancer immunotherapeutic.
Author List
Kharel A, Shen J, Brown R, Chen Y, Nguyen C, Alson D, Bluemn T, Fan J, Gai K, Zhang B, Kudek M, Zhu N, Cui WAuthors
Donia Alson Postdoctoral Researcher 2 in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinTheresa Bluemn Research Scientist II in the Pediatrics department at Medical College of Wisconsin
Matthew Kudek MD Assistant Professor in the Pediatrics department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsCD8-Positive T-Lymphocytes
Cell Differentiation
Humans
Melanoma
Mice
Transcription Factors
Virus Diseases









