ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Disparate roles for STAT5 in primary and secondary CTL responses.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Autocrine and paracrine IL-2 signals collaborate to regulate distinct phases of CD8 T cell memory.Cell reports · 2022Article
- Partial STAT5 signaling is sufficient for CD4Cytokine · 2022Article
- Mechanisms and consequences of Jak-STAT signaling in the immune system.Nature immunology · 2017Review
- The MicroRNA miR-191 Supports T Cell Survival Following Common γ Chain Signaling.The Journal of biological chemistry · 2016Article
- Cooperative therapeutic anti-tumor effect of IL-15 agonist ALT-803 and co-targeting soluble NKG2D ligand sMIC.Oncotarget · 2016Article
- Intrinsic Differences in Donor CD4 T Cell IL-2 Production Influence Severity of Parent-into-F1 Murine Lupus by Skewing the Immune Response Either toward Help for B Cells and a Sustained Autoantibody Response or toward Help for CD8 T Cells and a Downregulatory Th1 Response.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
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Authors and funding
2 authors.
Funding
Abstract
IL-2 signals during the primary response to infection are essential in shaping CD8(+) T cell fate decisions. How CD8(+) T cells integrate IL-2 signals in the development of functional memory is not well understood. Because IL-2 induces potent activation of the STAT5 transcription factor, we tested the role of STAT5 in CD8(+) memory T cell differentiation and function using a model system in which STAT5 activity is inducibly abrogated upon CD8(+) T cell activation. We report that STAT5 activity is broadly important for the expansion and effector function of all effector CTL subsets. After pathogen clearance, STAT5 was required for the survival of effector phenotype memory CTLs during the contraction phase. However, despite its role in supporting full primary CD8(+) T cell expansion, and unlike IL-2, STAT5 activity is not required for the development of memory CD8(+) T cells capable of robust secondary expansion upon rechallenge. Our findings highlight differential requirements for survival signals between primary and secondary effector CTL, and demonstrate that IL-2-dependent programming of memory CD8(+) T cells capable of secondary expansion and secondary effector differentiation is largely STAT5 independent.
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