ArticleCell death & disease2015
Smad4 represses the generation of memory-precursor effector T cells but is required for the differentiation of central memory T cells.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Smad4 and Eomes converge on a shared transcriptional program associated with inflammatory CD8 T-cell differentiation.Frontiers in immunology · 2026Article
- The diverse effects of transforming growth factor-β and SMAD signaling pathways during the CTL response.Frontiers in immunology · 2023Review
- CTLs Get SMAD When Pathogens Tell Them Where to Go.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- SMAD4 and TGFβ are architects of inverse genetic programs during fate determination of antiviral CTLs.eLife · 2022Article
- SMAD4, activated by the TCR-triggered MEK/ERK signaling pathway, critically regulates CD8Science advances · 2022Article
- The SUMOylation of TAB2 mediated by TRIM60 inhibits MAPK/NF-κB activation and the innate immune response.Cellular & molecular immunology · 2021Article
- Consequences of Mutations and Abnormal Expression of SMAD4 in Tumors and T Cells.OncoTargets and therapy · 2021Review
- Environmental cues orchestrate regional immune surveillance and protection by pulmonary CTLs.Journal of leukocyte biology · 2016Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional regulation underlying the differentiation of CD8(+) effector and memory T cells remains elusive. Here, we show that 18-month-old mice lacking the transcription factor Smad4 (homolog 4 of mothers against decapentaplegic, Drosophila), a key intracellular signaling effector for the TGF-β superfamily, in T cells exhibited lower percentages of CD44(hi)CD8(+) T cells. To explore the role of Smad4 in the activation/memory of CD8(+) T cells, 6- to 8-week-old mice with or without Smad4 in T cells were challenged with Listeria monocytogenes. Smad4 deficiency did not affect antigen-specific CD8(+) T-cell expansion but led to partially impaired cytotoxic function. Less short-lived effector T cells but more memory-precursor effector T cells were generated in the absence of Smad4. Despite that, Smad4 deficiency led to reduced memory CD8(+) T-cell responses. Further exploration revealed that the generation of central memory T cells was impaired in the absence of Smad4 and the cells showed survival issue. In mechanism, Smad4 deficiency led to aberrant transcriptional programs in antigen-specific CD8(+) T cells. These findings demonstrated an essential role of Smad4 in the control of effector and memory CD8(+) T-cell responses to infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.