Evidence map›Paper›PMID 22559987›Full record

ReviewSeminars in immunology2012

Changes in primary lymphoid organs with aging.

Ivan K Chinn, Clare C Blackburn, Nancy R Manley, Gregory D Sempowski

Abstract readReview
In one paragraph

Review in Seminars in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed
7.9field-weighted citation impact, top 2% of its field
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

156 citing papers in PubMed, 280 citations in OpenAlex.

  1. Trial
  2. Article
  3. What Do We Know About Immune System Aging from Human and Animal Studies?International journal of molecular sciences · 2026
    Review
  4. Article
  5. Review
  6. American Ginseng (Current issues in molecular biology · 2026
    Article
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96 more citing papers are in PubMed but not listed here.

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

4 authors at 4 institutions in 2 countries.

Ivan K ChinnDepartment of Pediatrics, Duke University Medical Center, Durham, NC 27710, USA.
Clare C Blackburn
Nancy R Manley
Gregory D Sempowski
Duke Medical Center · USDuke University Hospital · USUniversity of Edinburgh · GBUniversity of Georgia · US

Funding

Regional Biocontainment Laboratory (RBL)UC6AI058607 · NIAID · DUKE UNIVERSITY · PI WILLIAMS, R SANDERS · 2003 to 2005
$16.3M
Center for Molecular &Cellular Studies of Ped DiseaseK12HD043494 · NICHD · DUKE UNIVERSITY · PI REED, ANN M. · 2003 to 2017
$5.2M
Foxn1 and Molecular Mechanism of Thymic InvolutionR01AI082127 · NIAID · UNIVERSITY OF GEORGIA · PI MANLEY, NANCY R · 2009 to 2013
$2.0M
Mechanisms Controlling Thymic, Homeostasis, Involution, and ReboundP01AI076514 · NIAID · UNIVERSITY OF GEORGIA · PI MANLEY, NANCY R · 2009 to 2010
$2.0M
Regulation of thymic epithelial cell differentiationR01AI055001 · NIAID · UNIVERSITY OF GEORGIA (UGA) · PI MANLEY, NANCY R · 2003 to 2007
$1.6M
Mechanisms of Age Induced Thymic AtrophyR01AG025150 · NIA · DUKE UNIVERSITY · PI SEMPOWSKI, GREGORY D · 2005 to 2009
$1.5M
Steroid Receptors and Transcriptional Control of Thymic ReboundR01AG035302 · NIA · UNIVERSITY OF GEORGIA · PI BLACKBURN, CLARE, MANLEY, NANCY R · 2009 to 2011
$874k
Biotechnology and Biological Sciences Research Council BB/H021183/1NIAID NIH HHS AI076514NIAID NIH HHS AI082127NIAID NIH HHS HHSN272200900059CNIAID NIH HHS P01 AI076514NIAID NIH HHS R01 AI055001NIAID NIH HHS R01 AI082127NIAID NIH HHS UC6 AI058607NIA NIH HHS AG025150NIA NIH HHS AG035302NIA NIH HHS R01 AG025150NIA NIH HHS R01 AG035302NICHD NIH HHS HD043494NICHD NIH HHS K12 HD043494
6 · The paper itself

Abstract

Aging is associated with decreased immune function that leads to increased morbidity and mortality in the elderly. Immune senescence is accompanied by age-related changes in two primary lymphoid organs, bone marrow and thymus, that result in decreased production and function of B and T lymphocytes. In bone marrow, hematopoietic stem cells exhibit reduced self-renewal potential, increased skewing toward myelopoiesis, and decreased production of lymphocytes with aging. These functional sequelae of aging are caused in part by increased oxidative stress, inflammation, adipocyte differentiation, and disruption of hypoxic osteoblastic niches. In thymus, aging is associated with tissue involution, exhibited by a disorganization of the thymic epithelial cell architecture and increased adiposity. This dysregulation correlates with a loss of stroma-thymocyte 'cross-talk', resulting in decreased export of naïve T cells. Mounting evidence argues that with aging, thymic inflammation, systemic stress, local Foxn1 and keratinocyte growth factor expression, and sex steroid levels play critical roles in actively driving thymic involution and overall adaptive immune senescence across the lifespan. With a better understanding of the complex mechanisms and pathways that mediate bone marrow and thymus involution with aging, potential increases for the development of safe and effective interventions to prevent or restore loss of immune function with aging.

Indexed as

AgingAnimalsBone MarrowCell HypoxiaHumansImmunity, InnateLymphatic SystemOxidative Stress

Identifiers

PMID22559987
PMCPMC3415579
OpenAlexW2136991900

What OpenQuestion holds

Textmetadata
LicenceTDM
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.