Evidence map›Paper›PMID 24586170›Full record

ArticlePLoS pathogens2014

Engagement of NKG2D on bystander memory CD8 T cells promotes increased immunopathology following Leishmania major infection.

Erika J Crosby, Michael H Goldschmidt, E John Wherry, Phillip Scott

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

65 citing papers in PubMed, 93 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Bystander CD8Frontiers in immunology · 2025
    Article
  10. DAMP-ing IBD: Extinguish the Fire and Prevent Smoldering.Digestive diseases and sciences · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Lesional senescent CD4Frontiers in immunology · 2024
    Article
  17. IL-15-induced CD38Clinical & translational immunology · 2024
    Article
  18. Review
  19. Article
  20. Review

5 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

4 authors at 1 institution in 1 country.

Erika J CrosbyDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Michael H GoldschmidtDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
E John WherryDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Phillip ScottDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
University of Pennsylvania · US

Funding

Virology CoreU19AI082630 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI GEORG Michael LAUER · 2009 to 2026
$48.1M
The Impact of Bacterial Co-Infectin on Respiratory Virus-Specific T cell ResponseU19AI083022 · NIAID · WISTAR INSTITUTE · PI ERIKSON, JAN S. · 2009 to 2013
$10.7M
IL12 AS AN IMMUNOPOTENTIATOR IN LEISHMANIASISR01AI035914 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SCOTT, PHILLIP · 1994 to 2013
$4.5M
NIAID NIH HHS R01 AI035914NIAID NIH HHS U19 AI082630NIAID NIH HHS U19 AI083022PHS HHS R01 A135914
6 · The paper itself

Abstract

One of the hallmarks of adaptive immunity is the development of a long-term pathogen specific memory response. While persistent memory T cells certainly impact the immune response during a secondary challenge, their role in unrelated infections is less clear. To address this issue, we utilized lymphocytic choriomeningitis virus (LCMV) and Listeria monocytogenes immune mice to investigate whether bystander memory T cells influence Leishmania major infection. Despite similar parasite burdens, LCMV and Listeria immune mice exhibited a significant increase in leishmanial lesion size compared to mice infected with L. major alone. This increased lesion size was due to a severe inflammatory response, consisting not only of monocytes and neutrophils, but also significantly more CD8 T cells. Many of the CD8 T cells were LCMV specific and expressed gzmB and NKG2D, but unexpectedly expressed very little IFN-γ. Moreover, if CD8 T cells were depleted in LCMV immune mice prior to challenge with L. major, the increase in lesion size was lost. Strikingly, treating with NKG2D blocking antibodies abrogated the increased immunopathology observed in LCMV immune mice, showing that NKG2D engagement on LCMV specific memory CD8 T cells was required for the observed phenotype. These results indicate that bystander memory CD8 T cells can participate in an unrelated immune response and induce immunopathology through an NKG2D dependent mechanism without providing increased protection.

Indexed as

Immunologic MemoryLeishmania majorAnimalsCD8-Positive T-LymphocytesCytotoxicity, ImmunologicDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryLeishmaniasis, CutaneousLymphocyte ActivationLymphocytic ChoriomeningitisLymphocytic choriomeningitis virusMiceMice, Inbred C57BLNK Cell Lectin-Like Receptor Subfamily KKlrk1 protein, mouseNK Cell Lectin-Like Receptor Subfamily K

Identifiers

PMID24586170
PMCPMC3937277
OpenAlexW2075064711

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.