ArticleInfection and immunity2000
Activated T cells induce macrophages to produce NO and control Leishmania major in the absence of tumor necrosis factor receptor p55.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Characterization of the activation status of T lymphocyte subpopulations in peripheral blood from localized and diffused cutaneous leishmaniasis patients at the University of Gondar Hospital, Ethiopia.BMC infectious diseases · 2026Article
- Cytokine-Engineered Chimeric Antigen Receptor-T Cell Therapy: How to Balance the Efficacy and Toxicity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Arsenic exposure to mouse visceral leishmaniasis model through their drinking water linked to the disease exacerbation via modulation in host protective immunity: a preclinical study.Scientific reports · 2023Article
- The cytokine/chemokine response inHeliyon · 2023Review
- Cytokine release syndrome and associated neurotoxicity in cancer immunotherapy.Nature reviews. Immunology · 2022Review
- ChronicAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- The model of cytokine release syndrome in CAR T-cell treatment for B-cell non-Hodgkin lymphoma.Signal transduction and targeted therapy · 2020Review
- Review on the Role of Host Immune Response in Protection and Immunopathogenesis during Cutaneous Leishmaniasis Infection.Journal of immunology research · 2020Review
- Future Prospects in the Treatment of Parasitic Diseases: 2-Amino-1,3,4-Thiadiazoles in Leishmaniasis.Molecules (Basel, Switzerland) · 2019Review
- Article
- Genetic Manipulation of Leishmania donovani to Explore the Involvement of Argininosuccinate Synthase in Oxidative Stress Management.PLoS neglected tropical diseases · 2016Article
- Cigarette Smoke Induces Immune Responses to Vimentin in both, Arthritis-Susceptible and -Resistant Humanized Mice.PloS one · 2016Article
- CD40 and tumour necrosis factor-α co-operate to up-regulate inducuble nitric oxide synthase expression in macrophages.Immunology · 2012Article
- Protective immunity and vaccination against cutaneous leishmaniasis.Frontiers in immunology · 2012Article
- Characterization of chronic cutaneous lesions from TNF-receptor-1-deficient mice infected by Leishmania major.Clinical & developmental immunology · 2012Article
- CD40 and the immune response to parasitic infections.Seminars in immunology · 2009Review
- CD40 is required for the optimal induction of protective immunity to Mycobacterium avium.Immunology · 2004Article
- Defective localization of the NADPH phagocyte oxidase to Salmonella-containing phagosomes in tumor necrosis factor p55 receptor-deficient macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Influence of costimulatory molecules on immune response to Leishmania major by human cells in vitro.Infection and immunity · 2001Article
- Visceral leishmaniasis in mice devoid of tumor necrosis factor and response to treatment.Infection and immunity · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ability to activate macrophages in vitro for nitric oxide production and killing of Leishmania major parasites is dependent on tumor necrosis factor, although L. major-infected mice lacking the TNF receptor p55 (TNFRp55(-/-) mice) or both the TNFRp55 and TNFRp75 (TNFRp55p75(-/-) mice) are able to produce NO in vivo and eliminate the parasites. Here we report that activated T cells cocultured with macrophages results in TNFR-independent activation sufficient to control parasites and that both CD40/CD40L and LFA-1 contribute to T-cell-mediated macrophage activation. Thus, anti-CD3-stimulated T cells activated TNFR-deficient macrophages, while T cells from CD40L(-/-) mice were partially defective in triggering NO production by TNFRp55p75(-/-) macrophages. Moreover, in the presence of gamma interferon, anti-CD40 monoclonal antibody (MAb) activated TNFR-deficient macrophages. Finally, MAb blockade of LFA-1 completely inhibited macrophage NO production. Our data indicate that T cells can activate macrophages in the absence of TNF, thus providing a mechanism for how TNFR-deficient mice can control intracellular pathogens.
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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.