Evidence map›Paper›PMID 24610010›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Dendritic cell-MHC class II and Itk regulate functional development of regulatory innate memory CD4+ T cells in bone marrow transplantation.

Weishan Huang, Qian Qi, Jianfang Hu, Fei Huang, Terri M Laufer, Avery August

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  4. Review
  5. 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

6 authors at 3 institutions in 1 country.

Weishan HuangDepartment of Microbiology & Immunology and Program in Infection & Pathobiology, Cornell University, Ithaca, NY, USA.
Qian Qi *Department of Microbiology & Immunology and Program in Infection & Pathobiology, Cornell University, Ithaca, NY, USA.
Jianfang Hu *Huck Institutes of The Life Sciences and Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, PA, USA.
Fei HuangDepartment of Microbiology & Immunology and Program in Infection & Pathobiology, Cornell University, Ithaca, NY, USA.
Terri M LauferDepartment of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA.
Avery AugustDepartment of Microbiology & Immunology and Program in Infection & Pathobiology, Cornell University, Ithaca, NY, USA.
Cornell University · USPennsylvania State University · USUniversity of Pennsylvania · US

Funding

Tyrosine Kinase ITK in Experimental Allergic AsthmaR01AI051626 · NIAID · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI AUGUST, AVERY · 2003 to 2012
$3.6M
ITK Mast Cells and Allergic Airway ResponsesR01AI065566 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2007 to 2011
$1.5M
ITK Mast Cells and Allergic Airway ResponsesR56AI065566 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2006 to 2006
$345k
Eosinophils and Allergic Airway ResponsesR56AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2008
$61k
NIAID NIH HHS AI051626NIAID NIH HHS AI065566NIAID NIH HHS R01 AI051626NIAID NIH HHS R01 AI065566NIAID NIH HHS R56 AI065566NIAID NIH HHS R56 AI073955
6 · The paper itself

Abstract

MHC class II (MHCII)-influenced CD4(+) T cell differentiation and function play critical roles in regulating the development of autoimmunity. The lack of hematopoietic MHCII causes autoimmune disease that leads to severe wasting in syngeneic recipients. Using murine models of bone marrow transplantation (BMT), we find that MHCII(-/-)→wild-type BMT developed disease, with defective development of innate memory phenotype (IMP, CD44(hi)/CD62L(lo)) CD4(+) T cells. Whereas conventional regulatory T cells are unable to suppress pathogenesis, IMP CD4(+) T cells, which include conventional regulatory T cells, can suppress pathogenesis in MHCII(-/-)→wild-type chimeras. The functional development of IMP CD4(+) T cells requires hematopoietic but not thymic MHCII. B cells and hematopoietic CD80/86 regulate the population size, whereas MHCII expression by dendritic cells is sufficient for IMP CD4(+) T cell functional development and prevention of pathogenesis. Furthermore, the absence of Tec kinase IL-2-inducible T cell kinase in MHCII(-/-) donors leads to preferential development of IMP CD4(+) T cells and partially prevents pathogenesis. We conclude that dendritic cells-MHCII and IL-2-inducible T cell kinase regulate the functional development of IMP CD4(+) T cells, which suppresses the development of autoimmune disorder in syngeneic BMTs.

Indexed as

AnimalsBody WeightBone Marrow TransplantationCD4-Positive T-LymphocytesCell DifferentiationDendritic CellsFlow CytometryHistocompatibility Antigens Class IIHyaluronan ReceptorsImmunologic MemoryInterferon-gammaL-SelectinMiceMice, 129 StrainMice, Inbred C57BLMice, Knockoutemt protein-tyrosine kinaseHistocompatibility Antigens Class IIHyaluronan ReceptorsInterferon-gammaL-SelectinProtein-Tyrosine Kinases

Identifiers

PMID24610010
PMCPMC4033297
OpenAlexW1893492232

What OpenQuestion holds

Textmetadata
LicenceTDM
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.