Evidence map›Paper›PMID 18056355›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2007

LILRA2 activation inhibits dendritic cell differentiation and antigen presentation to T cells.

Delphine J Lee, Peter A Sieling, Maria Teresa Ochoa, Stephan R Krutzik, Beichu Guo, Maristela Hernandez, Thomas H Rea, Genhong Cheng, Marco Colonna, Robert L Modlin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

36 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Article
  3. NK Cells: A Powerful Squad Versus SARS-CoV-2.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. LILRB4, an immune checkpoint on myeloid cells.Blood science (Baltimore, Md.) · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Burn injury induces elevated inflammatory traffic: the role of NF-κB.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. In-silico modeling of granulomatous diseases.Current opinion in pulmonary medicine · 2016
    Review
  20. 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

10 authors at 3 institutions in 2 countries.

Delphine J LeeDivision of Dermatology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles 90095, USA.
Peter A Sieling
Maria Teresa Ochoa
Stephan R Krutzik
Beichu Guo
Maristela Hernandez
Thomas H Rea
Genhong Cheng
Marco Colonna
Robert L Modlin
University of California, Los Angeles · USWashington University in St. Louis · USUniversity of Southern California · US

Funding

Molecular Analysis of the Host Immune Response in LeprosyR01AI022553 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ROBERT L MODLIN · 1989 to 2026
$15.7M
TCR GAMMA/DELTA LYMPHOCYTES IN HUMAN SKIN LESIONSR01AR040312 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MODLIN, ROBERT L · 1990 to 2025
$10.4M
Viral Mediated Type I Interferon InductionR01AI069120 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHENG, GENHONG · 2006 to 2021
$6.0M
Mechanisms of Biodefense By Toll-Like ReceptorsR01AI056154 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHENG, GENHONG · 2004 to 2014
$3.7M
Leukocyte Immunoglobulin-like Receptors in Cutaneous Host DefenseK08AR053104 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEE, DELPHINE J · 2006 to 2010
$549k
IMMUNOREGULATORY T-LYMPHOCYTES IN LEPROSY SKIN LESIONSR22AI022553 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MODLIN, ROBERT L · 1986 to 1991
–
NIAID NIH HHS AI056154NIAID NIH HHS AI069120NIAID NIH HHS AI22553NIAID NIH HHS R01 AI022553NIAID NIH HHS R01 AI056154NIAID NIH HHS R01 AI069120NIAMS NIH HHS AR40312NIAMS NIH HHS K08 AR053104NIAMS NIH HHS R01 AR040312
6 · The paper itself

Abstract

The differentiation of monocytes into dendritic cells (DC) is a key mechanism by which the innate immune system instructs the adaptive T cell response. In this study, we investigated whether leukocyte Ig-like receptor A2 (LILRA2) regulates DC differentiation by using leprosy as a model. LILRA2 protein expression was increased in the lesions of the progressive, lepromatous form vs the self-limited, tuberculoid form of leprosy. Double immunolabeling revealed LILRA2 expression on CD14+, CD68+ monocytes/macrophages. Activation of LILRA2 on peripheral blood monocytes impaired GM-CSF induced differentiation into immature DC, as evidenced by reduced expression of DC markers (MHC class II, CD1b, CD40, and CD206), but not macrophage markers (CD209 and CD14). Furthermore, LILRA2 activation abrogated Ag presentation to both CD1b- and MHC class II-restricted, Mycobacterium leprae-reactive T cells derived from leprosy patients, while cytokine profiles of LILRA2-activated monocytes demonstrated an increase in TNF-alpha, IL-6, IL-8, IL-12, and IL-10, but little effect on TGF-beta. Therefore, LILRA2 activation, by altering GM-CSF-induced monocyte differentiation into immature DC, provides a mechanism for down-regulating the ability of the innate immune system to activate the adaptive T cell response while promoting an inflammatory response.

Indexed as

Antigen PresentationCell DifferentiationAntibodiesCells, CulturedCytokinesDendritic CellsGranulocyte-Macrophage Colony-Stimulating FactorHumansLymphocyte ActivationMonocytesReceptors, ImmunologicT-LymphocytesAntibodiesCytokinesGranulocyte-Macrophage Colony-Stimulating FactorLILRA2 protein, humanReceptors, Immunologic

Identifiers

PMID18056355
PMCPMC2650749
OpenAlexW1494826373

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.