Evidence map›Paper›PMID 15998789›Full record

ArticleThe Journal of experimental medicine2005

Restricted MHC-peptide repertoire predisposes to autoimmunity.

Nadezda N Logunova, Christophe Viret, Leonid A Pobezinsky, Sara A Miller, Dmitri B Kazansky, John P Sundberg, Alexander V Chervonsky

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

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  6. MHC-II alleles shape the CDR3 repertoires of conventional and regulatory naïve CD4Proceedings of the National Academy of Sciences of the United States of America · 2020
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  19. Development of CD4+ T cells expressing a nominally MHC class I-restricted T cell receptor by two different mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2006
    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

7 authors at 2 institutions in 1 country.

Nadezda N LogunovaThe Jackson Laboratory, Bar Harbor, ME 04609, USA.
Christophe Viret
Leonid A Pobezinsky
Sara A Miller
Dmitri B Kazansky
John P Sundberg
Alexander V Chervonsky
Jackson Laboratory · USYale University · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Biased Thymic Selection and Consequential AutoimmunityR01AI046782 · NIAID · UNIVERSITY OF CHICAGO · PI CHERVONSKY, ALEXANDER V · 2001 to 2005
$1.6M
MOUSE ALOPECIA AREATA: GENETICS AND MECHANISMSR01AR043801 · NIAMS · JACKSON LABORATORY · PI SUNDBERG, JOHN PAUL · 1997 to 2000
$205k
NCI NIH HHS CA 34196NCI NIH HHS P30 CA034196NIAID NIH HHS AI46782NIAID NIH HHS R01 AI046782NIAMS NIH HHS AR 43801
6 · The paper itself

Abstract

MHC molecules associated with autoimmunity possess known structural features that limit the repertoire of peptides that they can present. Such limitation gives a selective advantage to TCRs that rely on interaction with the MHC itself, rather than with the peptide residues. At the same time, negative selection is impaired because of the lack of negatively selecting peptide ligands. The combination of these factors may predispose to autoimmunity. We found that mice with an MHC class II-peptide repertoire reduced to a single complex demonstrated various autoimmune reactions. Transgenic mice bearing a TCR (MM14.4) cloned from such a mouse developed severe autoimmune dermatitis. Although MM14.4 originated from a CD4+ T cell, dermatitis was mediated by CD8+ T cells. It was established that MM14.4+ is a highly promiscuous TCR with dual MHC class I/MHC class II restriction. Furthermore, mice with a limited MHC-peptide repertoire selected elevated numbers of TCRs with dual MHC class I/MHC class II restriction, a likely source of autoreactivity. Our findings may help to explain the link between MHC class I responses that are involved in major autoimmune diseases and the well-established genetic linkage of these diseases with MHC class II.

Indexed as

AutoimmunityAnimalsAutoimmune DiseasesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesDermatitisHistocompatibility Antigens Class IHistocompatibility Antigens Class IIMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMice, KnockoutMice, TransgenicPeptidesReceptors, Antigen, T-CellHistocompatibility Antigens Class IHistocompatibility Antigens Class IIPeptidesReceptors, Antigen, T-Cell

Identifiers

PMID15998789
PMCPMC2212910
OpenAlexW2169980276

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.