The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.

Bcl-3 is an atypical member of the IκB family that acts in the nucleus to modulate transcription of many NF-κB targets in a highly context-dependent manner. Accordingly, complete Bcl-3-/- mice have diverse defects in both innate and adaptive immune responses; however, direct effects of Bcl-3 action...

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Main Authors: Hemant Jaiswal, Thomas Ciucci, Hongshan Wang, Wanhu Tang, Estefania Claudio, Philip M Murphy, Rémy Bosselut, Ulrich Siebenlist
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2021-01-01
Series:PLoS Pathogens
Online Access:https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1009249&type=printable
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author Hemant Jaiswal
Thomas Ciucci
Hongshan Wang
Wanhu Tang
Estefania Claudio
Philip M Murphy
Rémy Bosselut
Ulrich Siebenlist
author_facet Hemant Jaiswal
Thomas Ciucci
Hongshan Wang
Wanhu Tang
Estefania Claudio
Philip M Murphy
Rémy Bosselut
Ulrich Siebenlist
author_sort Hemant Jaiswal
collection DOAJ
description Bcl-3 is an atypical member of the IκB family that acts in the nucleus to modulate transcription of many NF-κB targets in a highly context-dependent manner. Accordingly, complete Bcl-3-/- mice have diverse defects in both innate and adaptive immune responses; however, direct effects of Bcl-3 action in individual immune cell types have not been clearly defined. Here, we document a cell-autonomous role for Bcl-3 in CD8+ T cell differentiation during the response to lymphocytic choriomeningitis virus infection. Single-cell RNA-seq and flow cytometric analysis of virus-specific Bcl3-/- CD8+ T cells revealed that differentiation was skewed towards terminal effector cells at the expense of memory precursor effector cells (MPECs). Accordingly, Bcl3-/- CD8+ T cells exhibited reduced memory cell formation and a defective recall response. Conversely, Bcl-3-overexpression in transgenic CD8+ T cells enhanced MPEC formation but reduced effector cell differentiation. Together, our results establish Bcl-3 as an autonomous determinant of memory/terminal effector cell balance during CD8+ T cell differentiation in response to acute viral infection. Our results provide proof-of-principle for targeting Bcl-3 pharmacologically to optimize adaptive immune responses to infectious agents, cancer cells, vaccines and other stimuli that induce CD8+ T cell differentiation.
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spelling doaj-art-ef2eb82acd264a7fb7589d5ab6025ba32025-08-20T02:23:18ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742021-01-01171e100924910.1371/journal.ppat.1009249The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.Hemant JaiswalThomas CiucciHongshan WangWanhu TangEstefania ClaudioPhilip M MurphyRémy BosselutUlrich SiebenlistBcl-3 is an atypical member of the IκB family that acts in the nucleus to modulate transcription of many NF-κB targets in a highly context-dependent manner. Accordingly, complete Bcl-3-/- mice have diverse defects in both innate and adaptive immune responses; however, direct effects of Bcl-3 action in individual immune cell types have not been clearly defined. Here, we document a cell-autonomous role for Bcl-3 in CD8+ T cell differentiation during the response to lymphocytic choriomeningitis virus infection. Single-cell RNA-seq and flow cytometric analysis of virus-specific Bcl3-/- CD8+ T cells revealed that differentiation was skewed towards terminal effector cells at the expense of memory precursor effector cells (MPECs). Accordingly, Bcl3-/- CD8+ T cells exhibited reduced memory cell formation and a defective recall response. Conversely, Bcl-3-overexpression in transgenic CD8+ T cells enhanced MPEC formation but reduced effector cell differentiation. Together, our results establish Bcl-3 as an autonomous determinant of memory/terminal effector cell balance during CD8+ T cell differentiation in response to acute viral infection. Our results provide proof-of-principle for targeting Bcl-3 pharmacologically to optimize adaptive immune responses to infectious agents, cancer cells, vaccines and other stimuli that induce CD8+ T cell differentiation.https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1009249&type=printable
spellingShingle Hemant Jaiswal
Thomas Ciucci
Hongshan Wang
Wanhu Tang
Estefania Claudio
Philip M Murphy
Rémy Bosselut
Ulrich Siebenlist
The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.
PLoS Pathogens
title The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.
title_full The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.
title_fullStr The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.
title_full_unstemmed The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.
title_short The NF-κB regulator Bcl-3 restricts terminal differentiation and promotes memory cell formation of CD8+ T cells during viral infection.
title_sort nf κb regulator bcl 3 restricts terminal differentiation and promotes memory cell formation of cd8 t cells during viral infection
url https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1009249&type=printable
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