ArticleThe Journal of experimental medicine2002
Treatment with soluble interleukin-15Ralpha exacerbates intracellular parasitic infection by blocking the development of memory CD8+ T cell response.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 51 citations in OpenAlex.
- IL-15 in T-Cell Responses and Immunopathogenesis.Immune network · 2024Review
- Impact of secondary TCR engagement on the heterogeneity of pathogen-specific CD8+ T cell response during acute and chronic toxoplasmosis.PLoS pathogens · 2022Article
- Functional roles of cytokines in infectious disease associated colorectal carcinogenesis.Molecular biology reports · 2022Review
- Influence of the Host and Parasite Strain on the Immune Response DuringFrontiers in cellular and infection microbiology · 2020Review
- Global Transcriptome Profiling of Multiple Porcine Organs RevealsFrontiers in immunology · 2019Article
- CD8+ T cell immunity in an encephalitis model of Toxoplasma gondii infection.Seminars in immunopathology · 2015Review
- Epidermal IL-15Rα acts as an endogenous antagonist of psoriasiform inflammation in mouse and man.The Journal of experimental medicine · 2013Article
- IL-7 and IL-15 do not synergize during CD8 T cell recall response against an obligate intracellular parasite.Microbes and infection · 2012Article
- The role of interleukin-15 in inflammation and immune responses to infection: implications for its therapeutic use.Microbes and infection · 2012Review
- The CD8 T-cell road to immunotherapy of toxoplasmosis.Immunotherapy · 2011Review
- CD8 T Cells and Toxoplasma gondii: A New Paradigm.Journal of parasitology research · 2011Article
- Absence of both IL-7 and IL-15 severely impairs the development of CD8 T cell response against Toxoplasma gondii.PloS one · 2010Article
- Subcellular expression pattern and role of IL-15 in pneumococci induced lung epithelial apoptosis.Histochemistry and cell biology · 2008Article
- Coinfection with Heligmosomoides polygyrus fails to establish CD8+ T-cell immunity against Toxoplasma gondii.Infection and immunity · 2008Article
- The immunology of parasite infections in immunocompromised hosts.Parasite immunology · 2006Review
- Coimmunization with IL-15 plasmid enhances the longevity of CD8 T cells induced by DNA encoding hepatitis B virus core antigen.World journal of gastroenterology · 2006Article
- CCR5 is essential for NK cell trafficking and host survival following Toxoplasma gondii infection.PLoS pathogens · 2006Article
- Lack of IL-15 results in the suboptimal priming of CD4+ T cell response against an intracellular parasite.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- NK cells help to induce CD8(+)-T-cell immunity against Toxoplasma gondii in the absence of CD4(+) T cells.Infection and immunity · 2005Article
- Induction of Mycobacterium tuberculosis-specific primary and secondary T-cell responses in interleukin-15-deficient mice.Infection and immunity · 2005Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Interferon (IFN)-gamma-producing CD8+ T cells are important for the successful resolution of the obligate intracellular parasite Toxoplasma gondii by preventing the reactivation or controlling a repeat infection. Previous reports from our laboratory have shown that exogenous interleukin (IL)-15 treatment augments the CD8+ T cell response against the parasite. However, the role of endogenous IL-15 in the proliferation of activated/memory CD8+ T cells during toxoplasma or any other infection is unknown. In this study, we treated T. gondii immune mice with soluble IL-15 receptor alpha (sIL-15Ralpha) to block the host endogenous IL-15. The treatment markedly reduced the ability of the immune animals to control a lethal infection. CD8+ T cell activities in the sIL-15Ralpha-administered mice were severely reduced as determined by IFN-gamma release and target cell lysis assays. The loss of CD8+ T cell immunity due to sIL-15Ralpha treatment was further demonstrated by adoptive transfer experiments. Naive recipients transferred with CD44(hi) activated/memory CD8+ T cells and treated with sIL-15Ralpha failed to resist a lethal T. gondii infection. Moreover, sIL-15Ralpha treatment of the recipients blocked the ability of donor CD44(hi) activated/memory CD8+ T cells to replicate in response to T. gondii challenge. To our knowledge, this is the first demonstration of the important role of host IL-15 in the development of antigen-specific memory CD8+ T cells against an intracellular infection.
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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.