ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Bid and Bim collaborate during induction of T cell death in persistent infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Polymorphisms within autophagy-related genes as susceptibility biomarkers for pancreatic cancer: A meta-analysis of three large European cohorts and functional characterization.International journal of cancer · 2025Pooled it
- Resolving the field: a role for Nod2 in T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- Engineering resilient CAR T cells for immunosuppressive environment.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- GFI1-driven transcriptional and epigenetic programs maintain CD8Nature immunology · 2025Article
- T Cell Resistance: On the Mechanisms of T Cell Non-activation.Immune network · 2024Review
- Site-specific transgene integration in chimeric antigen receptor (CAR) T cell therapies.Biomarker research · 2023Review
- BCL-2-family protein tBID can act as a BAX-like effector of apoptosis.The EMBO journal · 2022Article
- Hexokinases inhibit death receptor-dependent apoptosis on the mitochondria.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Rethinking peripheral T cell tolerance: checkpoints across a T cell's journey.Nature reviews. Immunology · 2021Review
- 4-1BB costimulation promotes CAR T cell survival through noncanonical NF-κB signaling.Science signaling · 2020Article
- Prolonged Persistence of Chimeric Antigen Receptor (CAR) T Cell in Adoptive Cancer Immunotherapy: Challenges and Ways Forward.Frontiers in immunology · 2020Review
- Caspase-8 restricts natural killer cell accumulation during MCMV Infection.Medical microbiology and immunology · 2019Article
- ERK1/2 and the Bcl-2 Family Proteins Mcl-1, tBid, and Bim Are Involved in Inhibition of Apoptosis During Persistent Chlamydia psittaci Infection.Inflammation · 2018Article
- The BCL-2 pro-survival protein A1 is dispensable for T cell homeostasis on viral infection.Cell death and differentiation · 2017Article
- Life and Death of Activated T Cells: How Are They Different from Naïve T Cells?Frontiers in immunology · 2017Review
- IL-12 and type I interferon prolong the division of activated CD8 T cells by maintaining high-affinity IL-2 signaling in vivo.The Journal of experimental medicine · 2014Article
- Guarding effector T-cell survival: all for one, Mcl-1 for all?Cell death and differentiation · 2013Article
- Regulation of antiviral CD8 T-cell responses.Critical reviews in immunology · 2013Review
- Apoptosis - an Ubiquitous T cell Immunomodulator.Journal of clinical & cellular immunology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Upon Ag encounter, naive T cells undergo extensive Ag-driven proliferation and can differentiate into effector cells. Up to 95% of these cells die leaving a small residual population of T cells that provide protective memory. In this study, we investigated the contribution of the BH3-only family protein Bid in the shutdown of T cell responses after acute and persistent infection. Influenza virus pathogenicity has been proposed to be mediated by a peptide encoded in the basic polymerase (PB1-RF2) acting through Bid. In our experiments, we found that after acute infection with influenza virus, mice lacking Bid had normal expansion and contraction of Ag-specific CD8(+) T cells. However, in chronic γ-herpesvirus infection, Bid-deficient virus-specific CD8(+) T cells expanded normally but failed to contract fully and were maintained at ∼2-fold higher levels. Previously, we have demonstrated that Bim plays a prominent role in T cell shutdown in persistent infection by cooperating with the death receptor Fas, which regulates apoptosis in response to repeated TCR signaling. Bid lies at the nexus of these two signaling pathways, thus we reasoned that Bid and Bim might cooperate in regulation of T cell shutdown in persistent infection. In this study, we observed that the combined loss of Bid and Bim synergistically enhanced the persistence of CD8(+) T cells during γ-herpesvirus infection. Thus, these data uncover a role for Bid in coordinating apoptotic signaling pathways to ensure appropriate shutdown of T cell immune responses in the setting of persistent Ag exposure.
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Registered trials
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