ArticleInfection and immunity2000
Visceral leishmaniasis in mice devoid of tumor necrosis factor and response to treatment.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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.
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.
Who cites it
56 citing papers in PubMed.
- Chemical degradation of Human p38-MAPK reveals it as a potential host target to combat parasitic infections by Leishmania donovani and Plasmodium falciparum.Communications biology · 2026Article
- New Advancements in the Field of Leishmaniasis.Microorganisms · 2026Article
- Interleukin-8 Predicts Fatal Kala-Azar: A Case-Control Study.Tropical medicine and infectious disease · 2025Article
- Leishmaniasis in Patients With Inflammatory Bowel Disease: A National Multicenter Study of GETECCU.United European gastroenterology journal · 2025Observational
- Innate biosignature of treatment failure in human cutaneous leishmaniasis.Nature communications · 2025Article
- Article
- Protein dysregulation duringFrontiers in immunology · 2025Article
- Innate biosignature of treatment failure in human cutaneous leishmaniasis.Research square · 2024Article
- Immunosuppressants alter the immune response associated with GlucantimeFrontiers in immunology · 2023Article
- Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection.Scientific reports · 2021Article
- Miltefosine enhances infectivity of a miltefosine-resistant Leishmania infantum strain by attenuating its innate immune recognition.PLoS neglected tropical diseases · 2021Article
- Potential biomarkers of immune protection in human leishmaniasis.Medical microbiology and immunology · 2021Review
- Immuno-pharmacokinetics of Meglumine Antimoniate in Patients With Cutaneous Leishmaniasis Caused by Leishmania (Viannia).Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Article
- Leucocytes and Th-associated Cytokine Profile of HIV-Leishmaniasis Co-Infected Persons Attending Abuja Teaching Hospital, Nigeria.The Eurasian journal of medicine · 2020Article
- Acute IL-4 Governs Pathogenic T Cell Responses duringImmunoHorizons · 2020Article
- Differential immune response modulation in early Leishmania amazonensis infection of BALB/c and C57BL/6 macrophages based on transcriptome profiles.Scientific reports · 2019Article
- Cytokines: Key Determinants of Resistance or Disease Progression in Visceral Leishmaniasis: Opportunities for Novel Diagnostics and Immunotherapy.Frontiers in immunology · 2019Review
- Article
- Gamma Interferon-Regulated Chemokines in Leishmania donovani Infection in the Liver.Infection and immunity · 2017Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Tumor necrosis factor (TNF)-deficient mice were challenged with Leishmania donovani to characterize TNF in the response of visceral intracellular infection to antileishmanial chemotherapy. In wild-type controls (i) liver infection peaked at week 2 and resolved, (ii) discrete liver granulomas developed at weeks 2 to 4 and involuted, and (iii) leishmanicidal responses to antimony (Sb), amphotericin B (AmB), and miltefosine were intact. In TNF knockout (KO) mice (i) initial liver infection was unrestrained, plateaued, and then declined somewhat by week 6, (ii) an absent early granulomatous reaction abruptly accelerated with striking tissue inflammation, widespread hepatic necrosis, and 100% mortality by week 10, and (iii) while the initial response to AmB and miltefosine was intact, killing induced by Sb therapy was reduced by >50%. Although initial AmB treatment during weeks 2 to 3 killed 98% of liver parasites, 75% of AmB-treated KO mice subsequently relapsed and died by week 12; however, additional maintenance AmB preserved long-term survival. These results for a model of visceral infection indicate that endogenous TNF is required early on to control intracellular L. donovani, support granuloma development, and mediate optimal initial effects of Sb and prevent relapse after ordinarily curative AmB treatment. A compensatory, TNF-independent antileishmanial mechanism developed in TNF KO mice; however, its effect was uncontrolled fatal inflammation. Chemotherapeutic elimination of the parasite stimulus reversed the hyperinflammatory response and preserved survival.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.