Evidence map›Paper›PMID 11519731›Full record

ReviewNeurochemical research2001

TCR peptide therapy in human autoimmune diseases.

A A Vandenbark, E Morgan, R Bartholomew, D Bourdette, R Whitham, D Carlo, D Gold, G Hashim, H Offner

Abstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
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  12. Autoimmune concepts of multiple sclerosis as a basis for selective immunotherapy: from pipe dreams to (therapeutic) pipelines.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Review
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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

9 authors at 3 institutions in 1 country.

A A VandenbarkNeuroimmunology Research, Veterans Affairs Medical Center, Portland, OR 97201, USA. vandenbark.arthur_a@portland.va.gov
E Morgan
R Bartholomew
D Bourdette
R Whitham
D Carlo
D Gold
G Hashim
H Offner
Oregon Health & Science University · USResponse Technologies (United States) · USPortland VA Medical Center · US

Funding

T LYMPHOCYTE LINES SPECIFIC FOR MYELIN BASIC PROTEINR01NS023221 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI VANDENBARK, ARTHUR A. · 1986 to 2010
$3.7M
REGULATION OF BASIC PROTEIN SPECIFIC T LYMPHOCYTE LINESR01NS023444 · NINDS · OREGON HEALTH AND SCIENCE UNIVERSITY · PI OFFNER, HALINA · 1987 to 2005
$3.0M
NINDS NIH HHS NS23221NINDS NIH HHS NS23444
6 · The paper itself

Abstract

Inflammatory Th1 cells reacting to tissue/myelin derived antigens likely contribute to the pathogenesis of diseases such as multiple sclerosis (MS), rheumatoid arthritis (RA), and psoriasis. One regulatory mechanism that may be useful for treating autoimmune diseases involves an innate second set of Th2 cells specific for portions of the T cell receptor of clonally expanded pathogenic Th1 cells. These Th2 cells are programmed to respond to internally modified V region peptides from the T cell receptor (TCR) that are expressed on the Th1 cell surface in association with major histocompatibility molecules. Once the regulatory Th2 cells are specifically activated, they may inhibit inflammatory Th1 cells through a non-specific bystander mechanism. A variety of strategies have been used by us to identify candidate disease-associated TCR V genes present on pathogenic Th1 cells, including BV5S2, BV6S5, and BV13SI in MS, BV3, BV14, and BV17 in RA, and BV3 and BV13S1 in psoriasis. TCR peptides corresponding to the mid region of these BV genes were found to be consistently immunogenic in vivo when administered either i.d. in saline or i.m. in incomplete Freund's adjuvant (IFA). In MS patients, repeated injection of low doses of peptides (100-300 microg) significantly boosted the number of TCR-reactive Th2 cells. These activated cells secreted cytokines, including IL-10, that are known to inhibit inflammatory Th1 cells. Cytokine release could also be induced in TCR-reactive Th2 cells by direct cell-cell contact with Th1 cells expressing the target V gene. These findings indicate the potential of regulatory Th2 cells to inhibit not only the target Th1 cells, but also bystander Th1 cells expressing different V genes specific for other autoantigens. TCR peptide vaccines have been used in our studies to treat a total of 171 MS patients (6 trials), 484 RA patients (7 trials), and 177 psoriasis patients (2 trials). Based on this experience in 824 patients with autoimmune diseases, TCR peptide vaccination is safe and well tolerated, and can produce significant clinical improvement in a subset of patients that respond to immunization. TCR peptide vaccination represents a promising approach that is well-suited for treating complex autoimmune diseases.

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesHumansMultiple SclerosisPeptide FragmentsPsoriasisReceptors, Antigen, T-CellPeptide FragmentsReceptors, Antigen, T-Cell

Identifiers

PMID11519731
OpenAlexW1597474270

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.