ArticleProceedings of the National Academy of Sciences of the United States of America2010
Ablation of SLP-76 signaling after T cell priming generates memory CD4 T cells impaired in steady-state and cytokine-driven homeostasis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- NRF2-mediated inhibition of alveolar macrophage MHC II expression during Mycobacterium tuberculosis infection.Cell reports · 2026Article
- Ibrutinib enhances the bias of T cell responses towards staphylococcal superantigens sustaining inflammation in chronic lymphocytic leukaemia.Frontiers in immunology · 2025Article
- A guide to adaptive immune memory.Nature reviews. Immunology · 2024Review
- T-cell receptor signal strength and epigenetic control of Bim predict memory CD8Cell death and differentiation · 2020Article
- Simulation of Stimulation: Cytokine Dosage and Cell Cycle Crosstalk Driving Timing-Dependent T Cell Differentiation.Frontiers in physiology · 2018Article
- Regulatory T cells require TCR signaling for their suppressive function.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- TCR Signaling in T Cell Memory.Frontiers in immunology · 2015Review
- Memory CD4 T cells in influenza.Current topics in microbiology and immunology · 2015Review
- Human memory T cells: generation, compartmentalization and homeostasis.Nature reviews. Immunology · 2014Review
- CD4 T-cell memory generation and maintenance.Critical reviews in immunology · 2014Review
- Signal transduction via the T cell antigen receptor in naïve and effector/memory T cells.The international journal of biochemistry & cell biology · 2012Review
- Homeostatic division is not necessary for antigen-specific CD4+ memory T cell persistence.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- TCR signaling requirements for activating T cells and for generating memory.Cellular and molecular life sciences : CMLS · 2012Review
- Conditional deletion of SLP-76 in mature T cells abrogates peripheral immune responses.European journal of immunology · 2011Article
- Transcriptional control of rapid recall by memory CD4 T cells.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- The memory phase of the CD4 T-cell response to influenza virus infection maintains its diverse antigen specificity.Immunology · 2011Article
- Loss of tonic T-cell receptor signals alters the generation but not the persistence of CD8+ memory T cells.Blood · 2010Article
- T-cell receptor signals direct the composition and function of the memory CD8+ T-cell pool.Blood · 2010Article
- Generation, persistence and plasticity of CD4 T-cell memories.Immunology · 2010Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The intracellular signaling mechanisms regulating the generation and long-term persistence of memory T cells in vivo remain unclear. In this study, we used mouse models with conditional deletion of the key T cell receptor (TCR)-coupled adaptor molecule SH2-domain-containing phosphoprotein of 76 kDa (SLP-76), to analyze signaling mechanisms for memory CD4 T cell generation, maintenance, and homeostasis. We found that ablation of SLP-76 expression after T cell priming did not inhibit generation of phenotypic effector or memory CD4 T cells; however, the resultant SLP-76-deficient memory CD4 T cells could not produce recall cytokines in response to TCR-mediated stimulation and showed decreased persistence in vivo. In addition, SLP-76-deficient memory CD4 T cells exhibited reduced steady-state homeostasis and were impaired in their ability to homeostatically expand in vivo in response to the gamma(c) cytokine IL-7, despite intact proximal signaling through the IL-7R-coupled JAK3/STAT5 pathway. Direct in vivo deletion of SLP-76 in polyclonal memory CD4 T cells likewise led to impaired steady-state homeostasis as well as impaired homeostatic responses to IL-7. Our findings demonstrate a dominant role for SLP-76-dependent TCR signals in regulating turnover and perpetuation of memory CD4 T cells and their responses to homeostatic cytokines, with implications for the selective survival of memory CD4 T cells following pathogen exposure, vaccination, and aging.
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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.