Evidence map›Paper›PMID 11444388›Full record

ReviewImmunologic research2001

Antigen-specific responses in autoimmunity and tolerance.

J W Thomas

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. 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

1 author at 1 institution in 1 country.

J W ThomasDivision of Rheumatology and Clinical Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-2681, USA. james.thomas@mcmail.vanderbilt.edu
Vanderbilt University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoantibodies to the hormone insulin arise spontaneously in the insulin autoimmune syndrome and in the prodrome of type I diabetes. Further, administration of insulin to individuals without autoimmune disease routinely results in antibodies that bind autologous hormone. These observations suggest that physiological levels of hormones, such as insulin, are below critical thresholds for signaling tolerance induction, a state termed clonal ignorance. In contrast, studies from our laboratory on the genetic origins and structure of V genes used by insulin antibodies suggest that the anti-insulin repertoire is tightly regulated. We have shown that B cells in mice harboring an insulin antibody transgene are functionally silenced. These findings verify that tolerance is active for small molecules, even when they are present at low concentrations. Despite active tolerance, insulin antibodies are sustained in the repertoire of normal animals by several mechanisms, including activation by TI antigen signals, unique display of conformational epitopes, and the recruitment of B cells previously selected by responses to other antigens. This essay reviews our current understanding of escape pathways for anti-insulin B cells.

Indexed as

AnimalsAntibody DiversityAutoantibodiesAutoantigensAutoimmune DiseasesAutoimmunityB-Lymphocyte SubsetsClonal AnergyDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1EpitopesFemaleFetal MacrosomiaGene Rearrangement, B-LymphocyteGene SilencingGenes, ImmunoglobulinAutoantibodiesAutoantigensEpitopesImmunoglobulin Variable RegionInsulin

Identifiers

PMID11444388
OpenAlexW1983838631

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.