Evidence map›Paper›PMID 41861249›Full record

ReviewCurrent opinion in hematology2026

Improving lymphopoiesis in aged bone marrow.

Anna Konturek-Ciesla, David Bryder

Abstract readReview
In one paragraph

Review in Current opinion in hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Anna Konturek-CieslaDepartment of Biosystems Science and Engineering, ETH Zurich, Basel, Switzerland.
David BryderDivision of Molecular Hematology, Lund Stem Cell Center, Lund University, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewAging is associated with impaired B lymphopoiesis and T lymphopoiesis, contributing to immunosenescence and poor immune recovery. Although this decline can be attributed to intrinsic hematopoietic stem cell aging, growing evidence indicates that lymphoid failure reflects constraints operating across multiple levels of the hematopoietic system. This review frames age-associated lymphopoiesis decline as a systems-level problem and outlines conceptual avenues for therapeutic intervention. RECENT

findingsAge-associated lymphoid failure is increasingly attributed to inflammatory suppression, dominance of dysfunctional stem and progenitor states, and compromised extramedullary support. These insights provide a framework for interventions that restore immune competence by rebalancing hematopoiesis or selectively replacing compromised stem cell function. SUMMARY: Age-associated lymphoid decline arises from coordinated constraints across the bone marrow niche, stem and progenitor composition, and extramedullary lymphoid support, rather than intrinsic stem cell exhaustion alone. Targeting these bottlenecks in a context-dependent manner offers multiple routes to improve lymphopoiesis and restore immune competence in aging.

Indexed as

AgingBone MarrowHematopoietic Stem CellsLymphopoiesisAnimalsB-LymphocytesCellular SenescenceHumansT-Lymphocyteshematopoietic stem and progenitor cellsimmune aginglymphopoiesisregeneration

Identifiers

PMID41861249
PMCPMC13236047

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.