ArticleThe Journal of experimental medicine2007
Memory CD8+ T cells mediate antibacterial immunity via CCL3 activation of TNF/ROI+ phagocytes.
Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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.
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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.
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Who cites it
51 citing papers in PubMed, 101 citations in OpenAlex.
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- Disrupting EDEM3-induced M2-like macrophage trafficking by glucose restriction overcomes resistance to PD-1/PD-L1 blockade.Clinical and translational medicine · 2025Article
- DNA architectural protein CTCF facilitates subset-specific chromatin interactions to limit the formation of memory CD8Immunity · 2023Article
- T-cell immunity to SARS-CoV-2: what if the known best is not the optimal course for the long run? Adapting to evolving targets.Frontiers in immunology · 2023Review
- Generation of Tumor Targeted Dendritic Cell Vaccines with Improved Immunogenic and Migratory Phenotype.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Memory CD8Science advances · 2021Article
- Development of a Simple and Robust Whole Blood Assay with Dual Co-Stimulation to Quantify the Release of T-Cellular Signature Cytokines in Response toJournal of fungi (Basel, Switzerland) · 2021Article
- Chemokine Signatures of Pathogen-Specific T Cells II: Memory T Cells in Acute and Chronic Infection.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- CD29 identifies IFN-γ-producing human CD8Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- CCL3/Macrophage Inflammatory Protein-1α Is Dually Involved in Parasite Persistence and Induction of a TNF- and IFNγ-Enriched Inflammatory Milieu inFrontiers in immunology · 2020Article
- Immune Response Resetting in Ongoing Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- The Uncovered Role of Immune Cells and NK Cells in the Regulation of Bone Metastasis.Frontiers in endocrinology · 2019Review
- Chemokines as adjuvants for immunotherapy: implications for immune activation with CCL3.Expert review of clinical immunology · 2017Review
- The Essential Role of Neutrophils during Infection with the Intracellular Bacterial Pathogen Listeria monocytogenes.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- Protective and Pathogenic Roles of CD8+ T Lymphocytes in Murine Orientia tsutsugamushi Infection.PLoS neglected tropical diseases · 2016Article
- Memory CD8(+) T Cells: Innate-Like Sensors and Orchestrators of Protection.Trends in immunology · 2016Review
- Snai2 and Snai3 transcriptionally regulate cellular fitness and functionality of T cell lineages through distinct gene programs.Immunobiology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytolysis, interferon gamma and tumor necrosis factor (TNF) alpha secretion are major effector mechanisms of memory CD8+ T cells that are believed to be required for immunological protection in vivo. By using mutants of the intracellular bacterium Listeria monocytogenes, we found that none of these effector activities is sufficient to protect against secondary infection with wild-type (WT) bacteria. We demonstrated that CCL3 derived from reactivated memory CD8+ T cells is required for efficient killing of WT bacteria. CCL3 induces a rapid TNF-alpha secretion by innate inflammatory mononuclear phagocytic cells (MPCs), which further promotes the production of radical oxygen intermediates (ROIs) by both MPCs and neutrophils. ROI generation is the final bactericidal mechanism involved in L. monocytogenes clearance. These results therefore uncover two levels of regulation of the antibacterial secondary protective response: (a) an antigen-dependent phase in which memory CD8+ T cells are reactivated and control the activation of the innate immune system, and (b) an antigen-independent phase in which the MPCs coordinate innate immunity and promote the bactericidal effector activities. In this context, CCL3-secreting memory CD8+ T cells are able to mediate "bystander" killing of an unrelated pathogen upon antigen-specific reactivation, a mechanism that may be important for the design of therapeutic vaccines.
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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.