Evidence map›Paper›PMID 40169598›Full record

ArticleNature communications2025

Kupffer cell and recruited macrophage heterogeneity orchestrate granuloma maturation and hepatic immunity in visceral leishmaniasis.

Gabriela Pessenda, Tiago R Ferreira, Andrea Paun, Juraj Kabat, Eduardo P Amaral, Olena Kamenyeva, Pedro Henrique Gazzinelli-Guimaraes, Shehan R Perera, Sundar Ganesan, Sang Hun Lee and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. 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. ApolipoproteinEiScience · 2026
    Article
  2. Review
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  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Gabriela PessendaLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Tiago R FerreiraLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-4894-1515
Andrea PaunLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Juraj KabatBiological Imaging Section, Research Technology Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Eduardo P AmaralLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-5465-8113
Olena KamenyevaBiological Imaging Section, Research Technology Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-6541-5616
Pedro Henrique Gazzinelli-GuimaraesLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-4932-2206
Shehan R PereraDepartment of Electrical and Computer Engineering, The Ohio State University, Columbus, OH, USA.
Sundar GanesanBiological Imaging Section, Research Technology Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Sang Hun LeeLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
David L SacksLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. dsacks@niaid.nih.gov.ORCID http://orcid.org/0000-0002-7557-3124

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In murine models of visceral leishmaniasis (VL), the parasitization of resident Kupffer cells (resKCs) drives early Leishmania infantum growth in the liver, leading to granuloma formation and subsequent parasite control. Using the chronic VL model, we demonstrate that polyclonal resKCs redistributed to form granulomas outside the sinusoids, creating an open sinusoidal niche that was gradually repopulated by monocyte-derived KCs (moKCs) acquiring a tissue specific, homeostatic profile. Early-stage granulomas predominantly consisted of CLEC4F

Indexed as

GranulomaKupffer CellsLeishmaniasis, VisceralLiverMacrophagesAnimalsDisease Models, AnimalFemaleLectins, C-TypeLeishmania infantumMiceMice, Inbred C57BLMice, KnockoutMonocytesNitric Oxide Synthase Type IIReceptors, CCR2Ccr2 protein, mouseLectins, C-TypeNitric Oxide Synthase Type IIReceptors, CCR2

Identifiers

PMID40169598
PMCPMC11961706

What OpenQuestion holds

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LicenceCC BY
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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.