Evidence map›Paper›PMID 15944296›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2005

Exacerbated susceptibility to infection-stimulated immunopathology in CD1d-deficient mice.

Stephen T Smiley, Paula A Lanthier, Kevin N Couper, Frank M Szaba, Jonathan E Boyson, Wangxue Chen, Lawrence L Johnson

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 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
3.1field-weighted citation impact, top 9% 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, 39 citations in OpenAlex.

  1. Article
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  7. Interleukin 23 in Crohn's disease.Inflammatory bowel diseases · 2014
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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

7 authors at 1 institution in 2 countries.

Stephen T SmileyTrudeau Institute, Inc., Saranac Lake, NY 12983, USA.
Paula A Lanthier
Kevin N Couper
Frank M Szaba
Jonathan E Boyson
Wangxue Chen
Lawrence L Johnson
University of Vermont · US

Funding

VERMONT IMMUNOBIOLOIGY/ INFECTIOUS DISEASES CENTERP20RR021905 · NCRR · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI HILL, JACK · 2006 to 2011
$14.5M
B CELL DEPENDENT IMMUNITY TO TOXOPLASMA GONDIIR01AI046571 · NIAID · TRUDEAU INSTITUTE, INC. · PI JOHNSON, LAWRENCE L. · 2000 to 2004
$1.9M
CD1D-Restricted T cells and Pregnancy LossR01AI067897 · NIAID · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BOYSON, JONATHAN E · 2007 to 2010
$1.5M
Roles for coagulation in immunityR01HL072937 · NHLBI · TRUDEAU INSTITUTE, INC. · PI SMILEY, STEPHEN T · 2002 to 2005
$1.4M
Regulation of innate immunity to infectionR21AI061587 · NIAID · TRUDEAU INSTITUTE, INC. · PI JOHNSON, LAWRENCE L. · 2004 to 2005
$700k
NCRR NIH HHS P20 RR021905NHLBI NIH HHS HL-72937NHLBI NIH HHS R01 HL072937NIAID NIH HHS AI-46571NIAID NIH HHS AI-61587NIAID NIH HHS R01 AI046571NIAID NIH HHS R01 AI067897NIAID NIH HHS R21 AI061587
6 · The paper itself

Abstract

Mice lacking functional CD1d genes were used to study mechanisms of resistance to the protozoan parasite Toxoplasma gondii. Wild-type (WT) BALB/c mice, CD1d-deficient BALB/c mice, and WT C57BL/6 mice all survived an acute oral infection with a low dose of mildly virulent strain ME49 T. gondii cysts. In contrast, most CD1d-deficient C57BL/6 mice died within 2 wk of infection. Despite having parasite burdens that were only slightly higher than WT mice, CD1d-deficient C57BL/6 mice displayed greater weight loss and intestinal pathology. In C57BL/6 mice, CD4(+) cells can cause intestinal pathology during T. gondii infection. Compared with WT mice, infected CD1d-deficient C57BL/6 mice had higher frequencies and numbers of activated (CD44(high)) CD4(+) cells in mesenteric lymph nodes. Depletion of CD4(+) cells from CD1d-deficient mice reduced weight loss and prolonged survival, demonstrating a functional role for CD4(+) cells in their increased susceptibility to T. gondii infection. CD1d-deficient mice are deficient in Valpha14(+) T cells, a major population of NKT cells. Involvement of these cells in resistance to T. gondii was investigated using gene-targeted Jalpha18-deficient C57BL/6 mice, which are deficient in Valpha14(+) T cells. These mice did not succumb to acute infection, but experienced greater weight loss and more deaths than B6 mice during chronic infection, indicating that Valpha14(+) cells contribute to resistance to T. gondii. The data identify CD4(+) cells as a significant component of the marked susceptibility to T. gondii infection observed in CD1d-deficient C57BL/6 mice, and establish T. gondii as a valuable tool for deciphering CD1d-dependent protective mechanisms.

Indexed as

Acute DiseaseAdministration, OralAnimalsAntibodies, MonoclonalAntigens, CD1Antigens, CD1dAntigens, ProtozoanCD4 AntigensCD4-Positive T-LymphocytesGenetic Predisposition to DiseaseImmunity, InnateIntestinal Diseases, ParasiticIntestinal MucosaMaleMiceMice, Inbred BALB CAntibodies, MonoclonalAntigens, CD1Antigens, CD1dAntigens, ProtozoanCD4 AntigensReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID15944296
PMCPMC3010175
OpenAlexW1509150189

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.