Evidence map›Paper›PMID 19522557›Full record

ReviewExpert opinion on biological therapy2009

Treating autoimmune disease by targeting CD8(+) T suppressor cells.

Christine Konya, Jorg J Goronzy, Cornelia M Weyand

Abstract readReview
In one paragraph

Review in Expert opinion on biological therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Characterization of novel CD8Cellular and molecular life sciences : CMLS · 2024
    Article
  2. Review
  3. CD8Frontiers in immunology · 2024
    Article
  4. Antigen perception in T cells by long-term Erk and NFAT signaling dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. CD8International journal of molecular sciences · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. CD8Frontiers in immunology · 2020
    Review
  11. Review
  12. Loss of Immune Tolerance Is Controlled by ICOS in Sle1 Mice.Journal of immunology (Baltimore, Md. : 1950) · 2016
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

3 authors.

Christine KonyaEmory University School of Medicine, Kathleen B. and Mason I. Lowance Center for Human Immunology and Rheumatology, Atlanta, GA 30322, USA.
Jorg J Goronzy
Cornelia M Weyand

Funding

VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
Atlanta Clinical and Translational Science Institute (ACTSI) RenewalUL1TR000454 · NCATS · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2012 to 2016
$25.8M
Vascular specific ACE expression and atherosclerosisP01HL058000 · NHLBI · VANDERBILT UNIVERSITY · PI DIKALOV, SERGEY · 1998 to 2013
$20.7M
Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
CD8 T CELLS IN RHEUMATOID SYNOVITISR01AI044142 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1999 to 2010
$2.9M
OCULAR DISEASE IN GIANT CELL ARTERITISR01EY011916 · NEI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1997 to 2011
$2.9M
DIVERSITY OF T LYMPHOCYTES IN RHEUMATOID ARTHRITISR01AR041974 · NIAMS · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI GORONZY, JORG J. · 1994 to 2006
$2.1M
T CELLS AND AGINGR01AG015043 · NIA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 1998 to 2008
$2.1M
NCATS NIH HHS UL1 TR000454NEI NIH HHS R01 EY011916NEI NIH HHS R01 EY11916NHLBI NIH HHS P01 HL058000NIAID NIH HHS R01 AI044142NIAID NIH HHS R01 AI44142NIAID NIH HHS U19 AI057266NIAID NIH HHS U19 AI57266NIAMS NIH HHS R01 AR041974NIAMS NIH HHS R01 AR042527NIAMS NIH HHS R01 AR41974NIAMS NIH HHS R01 AR42527NIA NIH HHS R01 AG015043NIA NIH HHS R01 AG15043
6 · The paper itself

Abstract

Current treatments for autoimmune disease are hampered by the non-specificity of immunomodulatory interventions, having to accept broad suppression of immunoresponsiveness with potentially serious side effects, such as infection or malignancy. The development of antigen-specific approaches, downregulating pathogenic immune responses while maintaining protective immunity, would be a major step forward. One possible approach involves the targeting of physiological regulatory mechanisms, such as inhibitory CD8 T cells that are now recognized to fine-tune many aspects of immune responses. CD8 T suppressor (Ts) cells may directly inhibit other T cells or condition antigen-presenting cells in such a way that immune amplification steps are dampened. The promise of CD8 Ts cells lies in their potential to disrupt host-injurious immune responses in a targeted fashion. For therapeutic purposes, such CD8 Ts cells could either be generated in vitro and transferred into the host or their numbers and activity could be modulated by treating the patient with established or novel immunomodulators. Emerging evidence shows that several subsets of CD8 Ts cells exist. While there is still considerable uncertainty about the molecular mechanisms through which CD8 Ts cells can reset immune responses to protect the host, their potential diagnostic and therapeutic use is intriguing and has generated renewed interest.

Indexed as

Allergy and ImmunologyAnimalsArthritis, RheumatoidAutoimmune DiseasesBiological TherapyCD8-Positive T-LymphocytesDiabetes Mellitus, Type 1HumansImmune SystemInflammatory Bowel DiseasesLupus Erythematosus, SystemicModels, BiologicalMultiple Sclerosis

Identifiers

PMID19522557
PMCPMC2790919

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.