Evidence map›Paper›PMID 12403361›Full record

ReviewImmunologic research2002

Specific deletion of autoreactive T cells by adenovirus-transfected, Fas ligand-producing antigen-presenting cells.

Huang-Ge Zhan, John D Mountz, Martin Fleck, Tong Zhou, Hui-Chen Hsu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Adenovirus-MediatedInternational journal of molecular sciences · 2020
    Article
  3. Article
  4. Killer B lymphocytes: the evidence and the potential.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2009
    Review
  5. Gene therapy of the rheumatic diseases: 1998 to 2008.Arthritis research & therapy · 2009
    Review
  6. Article
  7. Article
  8. 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

5 authors at 3 institutions in 2 countries.

Huang-Ge ZhanDepartment of Medicine, University of Alabama at Birmingham, 35294, USA.
John D Mountz
Martin Fleck
Tong Zhou
Hui-Chen Hsu
United States Department of Veterans Affairs · USUniversity of Alabama at Birmingham · USUniversity of Regensburg · DE

Funding

IN VIVO IMAGE ANALYSIS OF AUTOREACTIVE T CELLSR01AI046990 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 1999 to 2003
$2.0M
DEFECTIVE FAS APOPTOSIS DURING AGINGR01AG011653 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 1993 to 2005
$1.4M
GENE THERAPY TO CORRECT ARTHRITIS IN AUTOIMMUNE MICEN01AR062224 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 1996 to 2000
$328k
NIAID NIH HHS R01-AI-46990NIAMS NIH HHS N01 AR 6-2224NIA NIH HHS R01 AG 11653
6 · The paper itself

Abstract

Immune privilege is a unique strategy developed in several internal organs that can prevent the development of immune attack against these vital organs. One critical mechanism of immune privilege is utilization of Fas/FasL-mediated apoptosis to delete the invading T cells at the immune privilege sites. In this article, we describe the development and application of a unique cell-gene therapy to correct defective FasL-mediated apoptosis and autoimmune disease in autoimmune mice. This cell-gene therapy strategy using antigen-presenting cells (APCs) to express FasL is not only a therapeutic tool, but also has allowed us to understand the complexity of T cell regulation and the concept of eliminating T cells in the spleen, lymph node, or elsewhere in vivo to regulate the homeostasis of the peripheral T cell response. In this regard, the FasL-expressing APCs can be considered as circulating and regulatable immune privilege sites. Our studies provide substantial evidence that FasL-expressing APCs can be introduced exogenously without liver toxicity to eliminate infiltrating T cells and prevent the development of immune attack in lung, liver, kidney, joint, and salivary gland. Therefore, given the hazardous potential of persistent T cell invasion at the local inflammatory site, it is tempting to speculate that such an endogenous control mechanism occurs normally in vivo to limit a chronic T cell inflammatory response.

Indexed as

AutoimmunityAdenoviridaeAnimalsAntigen-Presenting CellsApoptosisFas Ligand Proteinfas ReceptorFemaleInflammationMaleMembrane GlycoproteinsMiceModels, ImmunologicalT-LymphocytesTransfectionFas Ligand ProteinFasl protein, mousefas ReceptorMembrane Glycoproteins

Identifiers

PMID12403361
OpenAlexW1989794554

What OpenQuestion holds

Textmetadata
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.