Evidence map›Paper›PMID 22972928›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Dendritic cell-specific disruption of TGF-β receptor II leads to altered regulatory T cell phenotype and spontaneous multiorgan autoimmunity.

Rajalakshmy Ramalingam, Claire B Larmonier, Robert D Thurston, Monica T Midura-Kiela, Song Guo Zheng, Fayez K Ghishan, Pawel R Kiela

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

81 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Review
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  7. Cytokines in transplantation tolerance.Best practice & research. Clinical haematology · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  13. Review
  14. Review
  15. Review
  16. Vitamin DInternational journal of molecular sciences · 2023
    Review
  17. Review
  18. Review
  19. Article
  20. Review

21 more citing papers are in PubMed but not listed here.

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.

Rajalakshmy RamalingamDepartment of Pediatrics, Steele Children's Research Center, University of Arizona, Tucson, AZ 85724, USA.
Claire B Larmonier
Robert D Thurston
Monica T Midura-Kiela
Song Guo Zheng
Fayez K Ghishan
Pawel R Kiela
University of Arizona · USUniversity of Southern California · US

Funding

Intestinal Barrier Function: Protective Effects of CurcuminR01DK067286 · NIDDK · UNIVERSITY OF ARIZONA · PI GHISHAN, FAYEZ KHALAF, KIELA, PAWEL R · 2005 to 2013
$2.6M
NIDDK NIH HHS 5R01DK067286NIDDK NIH HHS R01 DK067286
6 · The paper itself

Abstract

In vitro data and transgenic mouse models suggest a role for TGF-β signaling in dendritic cells (DCs) to prevent autoimmunity primarily through maintenance of DCs in their immature and tolerogenic state characterized by low expression of MHC class II (MHCII) and costimulatory molecules and increased expression of IDO, among others. To test whether a complete lack of TGF-β signaling in DCs predisposes mice to spontaneous autoimmunity and to verify the mechanisms implicated previously in vitro, we generated conditional knockout (KO) mice with Cre-mediated DC-specific deletion of Tgfbr2 (DC-Tgfbr2 KO). DC-Tgfbr2 KO mice die before 15 wk of age with multiorgan autoimmune inflammation and spontaneous activation of T and B cells. Interestingly, there were no significant differences in the expression of MHCII, costimulatory molecules, or IDO in secondary lymphoid organ DCs, although Tgfbr2-deficient DCs were more proinflammatory in vitro and in vivo. DC-Tgfbr2 KO showed attenuated Foxp3 expression in regulatory T cells (Tregs) and abnormal expansion of CD25(-)Foxp3(+) Tregs in vivo. Tgfbr2-deficient DCs secreted elevated levels of IFN-γ and were not capable of directing Ag-specific Treg conversion unless in the presence of anti-IFN-γ blocking Ab. Adoptive transfer of induced Tregs into DC-Tgfbr2 KO mice partially rescued the phenotype. Therefore, in vivo, TGF-β signaling in DCs is critical in the control of autoimmunity through both Treg-dependent and -independent mechanisms, but it does not affect MHCII and costimulatory molecule expression.

Indexed as

AnimalsAutoimmune DiseasesColitisDendritic CellsDisease Models, AnimalImmune ToleranceImmunophenotypingMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicOrgan SpecificityProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type II

Identifiers

PMID22972928
PMCPMC3466393
OpenAlexW2161264054

What OpenQuestion holds

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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.