ArticleJCI insight2020
Bone marrow is the preferred site of memory CD4+ T cell proliferation during recovery from sepsis.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Single-cell transcriptomic analysis reveals immune remodeling in bone marrow during aged sepsis.GeroScience · 2026Article
- The interplay between recovery and immunity in infectious and non-communicable diseases.Frontiers in cellular and infection microbiology · 2026Review
- Sepsis-induced inflammasome impairment facilitates development of secondaryEmerging microbes & infections · 2025Article
- Multi-omic analysis of PBMCs in sepsis reveals widespread cytotoxic dysfunction and an increased population ofFrontiers in immunology · 2025Article
- Reassessing sepsis research: new clues for old players and new players for an old symptom to improve patient outcomes.EXCLI journal · 2025Review
- Pharmacological and genetic inhibition of ARG2 in CXCR2Theranostics · 2025Article
- Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024Review
- Compartmentalization of the inflammatory response during bacterial sepsis and severe COVID-19.Journal of intensive medicine · 2024Review
- Unveiling Dynamic Changes and Regulatory Mechanisms of T Cell Subsets in Sepsis Pathogenesis.ImmunoTargets and therapy · 2024Article
- Advances in the Study of Immunosuppressive Mechanisms in Sepsis.Journal of inflammation research · 2023Review
- Keeping T cell memories in mind.Trends in immunology · 2022Review
- Sepsis-induced immunosuppression: mechanisms, diagnosis and current treatment options.Military Medical Research · 2022Review
- TLR2-induced CD8Frontiers in immunology · 2022Article
- Sepsis and multiple sclerosis: Causative links and outcomes.Immunology letters · 2021Review
- Lymphohematopoietic graft-versus-host responses promote mixed chimerism in patients receiving intestinal transplantation.The Journal of clinical investigation · 2021Article
- An Early Myelosuppression in the Acute Mouse Sepsis Is Partly Outcome-Dependent.Frontiers in immunology · 2021Article
- Sepsis impedes EAE disease development and diminishes autoantigen-specific naive CD4 T cells.eLife · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis survivors suffer from increased vulnerability to infections, and lymphopenia presumably contributes to this problem. The mechanisms of the recovery of memory CD4+ T cells after sepsis remain elusive. We used the cecal ligation and puncture mouse model of sepsis to study the restoration of the memory CD4+ T cells during recovery from sepsis. Then, adoptive transfer of antigen-specific naive CD4+ T cells followed by immunization and BrdU labeling were performed to trace the proliferation and migration of memory CD4+ T cells. We revealed that the bone marrow (BM) is the primary site of CD4+ memory T cell homing and proliferation after sepsis-induced lymphopenia. Of interest, BM CD4+ T cells had a higher basal proliferation rate in comparison with splenic T cells. These cells also show features of resident memory T cells yet have the capacity to migrate outside the BM niche and engraft secondary lymphoid organs. The BM niche also sustains viability and functionality of CD4+ T cells. We also identified IL-7 as the major inducer of proliferation of the BM memory CD4+ T cells and showed that recombinant IL-7 improves the recovery of these cells. Taken together, we provide data on the mechanism and location of memory CD4+ T cell proliferation during recovery from septic lymphopenia, which are of relevance in studying immunostimulatory therapies in sepsis.
Indexed as
Identifiers
What OpenQuestion holds
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.