Evidence map›Paper›PMID 19795459›Full record

ArticleInternational journal of cancer2010

Unifying roles for regulatory T cells and inflammation in cancer.

Susan E Erdman, Varada P Rao, Werner Olipitz, Christie L Taylor, Erin A Jackson, Tatiana Levkovich, Chung-Wei Lee, Bruce H Horwitz, James G Fox, Zhongming Ge and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

52 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Silicone breast implant-associated pathologies and T cell-mediated responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Translocation ofOncoimmunology · 2022
    Article
  9. Review
  10. Probiotics in Cancer.Frontiers in oncology · 2021
    Review
  11. Review
  12. Involvement ofInternational journal of molecular sciences · 2020
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Susan E ErdmanDivision of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. serdman@mit.edu
Varada P Rao
Werner Olipitz
Christie L Taylor
Erin A Jackson
Tatiana Levkovich
Chung-Wei Lee
Bruce H Horwitz
James G Fox
Zhongming Ge
Theofilos Poutahidis
Massachusetts Institute of Technology · USHarvard University · US

Funding

Reaction and Diffusion of NO in Biological SystemsP01CA026731 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI TANNENBAUM, STEVEN R · 1985 to 2018
$25.4M
POSTDOCTORAL TRAINING IN COMPARATIVE MEDICINET32RR007036 · NCRR · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI FOX, JAMES G · 1988 to 2011
$3.6M
Role of IL10 and TGFb1 in colon cancerR01CA108854 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ERDMAN, SUSAN E · 2005 to 2014
$2.4M
NCI NIH HHS P01 CA026731NCI NIH HHS P01CA26731NCI NIH HHS R01 CA108854NCI NIH HHS R01CA108854NCRR NIH HHS T32 RR007036NCRR NIH HHS T32RR07036
6 · The paper itself

Abstract

Activities of CD4(+) regulatory (T(REG)) cells restore immune homeostasis during chronic inflammatory disorders. Roles for T(REG) cells in inflammation-associated cancers, however, are paradoxical. It is widely believed that T(REG) function in cancer mainly to suppress protective anticancer responses. However, we demonstrate here that T(REG) cells also function to reduce cancer risk throughout the body by efficiently downregulating inflammation arising from the gastrointestinal (GI) tract. Building on a "hygiene hypothesis" model in which GI infections lead to changes in T(REG) that reduce immune-mediated diseases, here we show that gut bacteria-triggered T(REG) may function to inhibit cancer even in extraintestinal sites. Ability of bacteria-stimulated T(REG) to suppress cancer depends on interleukin (IL)-10, which serves to maintain immune homeostasis within bowel and support a protective antiinflammatory T(REG) phenotype. However, under proinflammatory conditions, T(REG) may fail to provide antiinflammatory protection and instead contribute to a T helper (Th)-17-driven procarcinogenic process; a cancer state that is reversible by downregulation of inflammation. Consequently, hygienic individuals with a weakened IL-10 and T(REG)-mediated inhibitory loop are highly susceptible to the carcinogenic consequences of elevated IL-6 and IL-17 and show more frequent inflammation-associated cancers. Taken together, these data unify seemingly divergent disease processes such as autoimmunity and cancer and help explain the paradox of T(REG) and inflammation in cancer. Enhancing protective T(REG) functions may promote healthful longevity and significantly reduce risk of cancer.

Indexed as

Disease Models, AnimalAdenomatous Polyposis Coli ProteinAnimalsBlotting, WesternCytokinesDNA-Binding ProteinsErb-b2 Receptor Tyrosine KinasesFemaleFlow CytometryHelicobacter hepaticusHelicobacter InfectionsImmunoenzyme TechniquesInflammationInterleukin-10Mammary Neoplasms, AnimalMiceAdenomatous Polyposis Coli ProteinCytokinesDNA-Binding ProteinsErbb2 protein, mouseErb-b2 Receptor Tyrosine KinasesInterleukin-10Rag2 protein, mouseRNA, Messenger

Identifiers

PMID19795459
PMCPMC4068029
OpenAlexW2064212629

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.