ArticleThe Journal of clinical investigation2015
An NLRP3 inflammasome-triggered Th2-biased adaptive immune response promotes leishmaniasis.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 134 citations in OpenAlex.
- An Immunocompetent Hepatic Organoid Model Reveals Conserved Hepatic Immune Dysregulation DuringInternational journal of molecular sciences · 2026Article
- Anisodus tanguticus in Cancer Research: A Review of Traditional Use, Phytochemistry, Extraction Methods, and Preclinical Antitumor Evidence.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- IL-18 favors Th2 responses in sporotrichosis caused by Sporothrix globosa, prolonging the course of the disease.PLoS neglected tropical diseases · 2025Article
- Transcriptomic and Immunopathological Profiles of Inflammasomes in Different Clinical Forms of American Cutaneous Leishmaniasis.Microorganisms · 2025Article
- A newly developed oral infection mouse model of shigellosis for immunogenicity and protective efficacy studies of a candidate vaccine.Infection and immunity · 2025Article
- NOD-like receptors in fish: evolution, structure, immune signaling, and targeting for aquaculture vaccine adjuvants.Frontiers in immunology · 2025Review
- Caspase-1 Variants and Plasma IL-1β in Patients withInternational journal of molecular sciences · 2024Article
- Molecular regulation of NLRP3 inflammasome activation during parasitic infection.Bioscience reports · 2024Review
- The non-pathogenic protozoonFrontiers in immunology · 2024Article
- The effects of Leishmania RNA virus 2 (LRV2) on the virulence factors of L. major and pro-inflammatory biomarkers: an in vitro study on human monocyte cell line (THP-1).BMC microbiology · 2023Article
- Icariin restrains NLRP3 inflammasome-mediated Th2 immune responses and ameliorates atopic dermatitis through modulating a novel lncRNA MALAT1/miR-124-3p axis.Pharmaceutical biology · 2023Article
- Emulsion and liposome-based adjuvanted R21 vaccine formulations mediate protection against malaria through distinct immune mechanisms.Cell reports. Medicine · 2023Article
- Regulatory Functions of Hypoxia in Host-Parasite Interactions: A Focus on Enteric, Tissue, and Blood Protozoa.Microorganisms · 2023Review
- Variants of CARD8 in Leishmania guyanensis-cutaneous leishmaniasis and influence of the variants genotypes on circulating plasma cytokines IL-1β, TNFα and IL-8.PLoS neglected tropical diseases · 2023Article
- Impavido attenuates inflammation, reduces atherosclerosis, and alters gut microbiota in hyperlipidemic mice.iScience · 2023Article
- Gasdermin-D activation promotes NLRP3 activation and host resistance to Leishmania infection.Nature communications · 2023Article
- Article
- The pathogenicity and virulence of Leishmania - interplay of virulence factors with host defenses.Virulence · 2022Review
- Eosinophils, but Not Type 2 Innate Lymphoid Cells, Are the Predominant Source of Interleukin 4 during the Innate Phase ofPathogens (Basel, Switzerland) · 2022Article
- The Interactions Between Autoinflammation and Type 2 Immunity: From Mechanistic Studies to Epidemiologic Associations.Frontiers in immunology · 2022Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Leishmaniasis is a major tropical disease that can present with cutaneous, mucocutaneous, or visceral manifestation and affects millions of individuals, causing substantial morbidity and mortality in third-world countries. The development of a Th1-adaptive immune response is associated with resistance to developing Leishmania major (L. major) infection. Inflammasomes are key components of the innate immune system that contribute to host defense against bacterial and viral pathogens; however, their role in regulating adaptive immunity during infection with protozoan parasites is less studied. Here, we demonstrated that the NLRP3 inflammasome balances Th1/Th2 responses during leishmaniasis. Mice lacking the inflammasome components NLRP3, ASC, or caspase 1 on a Leishmania-susceptible BALB/c background exhibited defective IL-1β and IL-18 production at the infection site and were resistant to cutaneous L. major infection. Moreover, we determined that production of IL-18 propagates disease in susceptible BALB/c mice by promoting the Th2 cytokine IL-4, and neutralization of IL-18 in these animals reduced L. major titers and footpad swelling. In conclusion, our results indicate that activation of the NLRP3 inflammasome is detrimental during leishmaniasis and suggest that IL-18 neutralization has potential as a therapeutic strategy to treat leishmaniasis patients.
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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.