Evidence map›Paper›PMID 38709823›Full record

ArticlePLoS pathogens2024

CCR5 promotes the migration of pathological CD8+ T cells to the leishmanial lesions.

Laís Amorim Sacramento, Camila Farias Amorim, Claudia G Lombana, Daniel Beiting, Fernanda Novais, Lucas P Carvalho, Edgar M Carvalho, Phillip Scott

Abstract read
In one paragraph

Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Evolving role of CD8Frontiers in immunology · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Oxygen and immunity toInfection and immunity · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Laís Amorim SacramentoDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Camila Farias AmorimDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Claudia G LombanaDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Daniel BeitingDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Fernanda NovaisDepartment of Microbial Infection and Immunity, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America.
Lucas P CarvalhoLaboratório de Pesquisas Clínicas do Instituto de Pesquisas Gonçalo Muniz-Fiocruz, Salvador, Bahia, Brazil.
Edgar M CarvalhoLaboratório de Pesquisas Clínicas do Instituto de Pesquisas Gonçalo Muniz-Fiocruz, Salvador, Bahia, Brazil.
Phillip ScottDepartment of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0001-8732-0653

Funding

The role of Leishmania braziliensis strain polymorphism on disease outcome and ..P50AI030639 · NIAID · FEDERAL UNIVERSITY OF BAHIA · PI CARVALHO, EDGAR M · 1991 to 2023
$9.1M
Skin microbiome contributions to the pathogenesis of cutaneous leishmaniasisR01AI143790 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI Elizabeth Anne Grice, PHILLIP SCOTT · 2019 to 2026
$6.0M
CD8 T cell-dependent pathways leading to immunopathology in cutaneous leishmaniasisR01AI150606 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI SCOTT, PHILLIP · 2020 to 2024
$2.8M
Distinct functions for CD8 T cells in cutaneous leishmaniasisR01AI162711 · NIAID · OHIO STATE UNIVERSITY · PI Fernanda Novais · 2022 to 2026
$2.1M
Host and parasite factors promoting disease and treatment failure in Leishmania braziliensis patientsR01AI149456 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI CARVALHO, LUCAS P, SCOTT, PHILLIP · 2020 to 2023
$626k
Parasite polymorphism and host immune response in cutaneous leishmaniasis outcomeR01AI136862 · NIAID · FEDERAL UNIVERSITY OF BAHIA · PI CARVALHO, LUCAS P, SCOTT, PHILLIP · 2018 to 2022
$593k
NIAID NIH HHS P50 AI030639NIAID NIH HHS R01 AI136862NIAID NIH HHS R01 AI143790NIAID NIH HHS R01 AI149456NIAID NIH HHS R01 AI150606NIAID NIH HHS R01 AI162711
6 · The paper itself

Abstract

Cytolytic CD8+ T cells mediate immunopathology in cutaneous leishmaniasis without controlling parasites. Here, we identify factors involved in CD8+ T cell migration to the lesion that could be targeted to ameliorate disease severity. CCR5 was the most highly expressed chemokine receptor in patient lesions, and the high expression of CCL3 and CCL4, CCR5 ligands, was associated with delayed healing of lesions. To test the requirement for CCR5, Leishmania-infected Rag1-/- mice were reconstituted with CCR5-/- CD8+ T cells. We found that these mice developed smaller lesions accompanied by a reduction in CD8+ T cell numbers compared to controls. We confirmed these findings by showing that the inhibition of CCR5 with maraviroc, a selective inhibitor of CCR5, reduced lesion development without affecting the parasite burden. Together, these results reveal that CD8+ T cells migrate to leishmanial lesions in a CCR5-dependent manner and that blocking CCR5 prevents CD8+ T cell-mediated pathology.

Indexed as

CD8-Positive T-LymphocytesCell MovementLeishmaniasis, CutaneousReceptors, CCR5AnimalsCCR5 Receptor AntagonistsFemaleHumansMaravirocMiceMice, Inbred C57BLMice, KnockoutCCR5 protein, humanCCR5 protein, mouseCCR5 Receptor AntagonistsMaravirocReceptors, CCR5

Identifiers

PMID38709823
PMCPMC11098486

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.