ArticleInfection and immunity2005
Invariant NKT cells are essential for the regulation of hepatic CXCL10 gene expression during Leishmania donovani infection.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Chemokines Signature and T Cell Dynamics in Leishmaniasis: Molecular insight and therapeutic application.Expert reviews in molecular medicine · 2024Review
- Early Transcriptional Liver Signatures in Experimental Visceral Leishmaniasis.International journal of molecular sciences · 2021Article
- The Potent ITK/BTK Inhibitor Ibrutinib Is Effective for the Treatment of Experimental Visceral Leishmaniasis Caused by Leishmania donovani.The Journal of infectious diseases · 2019Article
- Macrophage Transactivation for Chemokine Production Identified as a Negative Regulator of Granulomatous Inflammation Using Agent-Based Modeling.Frontiers in immunology · 2018Article
- Lessons from other diseases: granulomatous inflammation in leishmaniasis.Seminars in immunopathology · 2016Review
- Regulation of immunity during visceral Leishmania infection.Parasites & vectors · 2016Review
- Interferon gamma in leishmaniasis.Frontiers in immunology · 2013Article
- Functional complexity of the Leishmania granuloma and the potential of in silico modeling.Frontiers in immunology · 2013Article
- Article
- Interferon regulatory factor 7 contributes to the control of Leishmania donovani in the mouse liver.Infection and immunity · 2011Article
- Role of chemokines in regulation of immunity against leishmaniasis.Experimental parasitology · 2010Review
- Leishmania donovani-induced expression of signal regulatory protein alpha on Kupffer cells enhances hepatic invariant NKT-cell activation.European journal of immunology · 2010Article
- NKT cell immune responses to viral infection.Expert opinion on therapeutic targets · 2009Review
- Activation of invariant NKT cells exacerbates experimental visceral leishmaniasis.PLoS pathogens · 2008Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Gamma interferon (IFN-gamma)-regulated chemokines of the CXC family have been implicated as key regulators of a variety of T-cell-dependent inflammatory processes. However, the cellular source(s) of IFN-gamma that regulates their early expression has rarely been defined. Here, we have directly addressed this question in mice after Leishmania donovani infection. Comparison of CXCL10 mRNA accumulation in normal and IFN-gamma-deficient mice confirmed an absolute requirement for IFN-gamma for sustained (24 h) expression of CXCL10 mRNA accumulation in this model. In normal mice, IFN-gamma was produced by both CD3int NK1.1+ NKT cells and CD3- NK1.1+ NK cells, as detected by intracellular flow cytometry. Strikingly, B6.Jalpha281-/- mice lacking NKT cells that express the invariant Valpha14Jalpha18 T-cell-receptor alpha chain, although retaining a significant population of IFN-gamma-producing NK cells and NKT cells, were unable to sustain CXCL10 mRNA accumulation. These data indicate that invariant NKT cells are indispensable for the regulation of hepatic CXCL10 gene expression during L. donovani infection.
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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.