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Talia S Dalzell on Muck Rack

Talia S Dalzell

As seen in: BioRxiv, Cell Press
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Articles

Collaboration between interleukin-7 and -15 enables adaptation of tissue-resident and circulating memory CD8+ T cells to cytokine deficiency

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By Nicholas N Jarjour, Talia S Dalzell, Nicholas J. Maurice, Kelsey M. Wanhainen, Changwei Peng, Stephen D. O’Flanagan, Taylor A DePauw, Katharine E. Block, William J. Valente, K. Ashby, David Masopust, Stephen C Jameson
| Cell Press Verified
Keywords adaptive immunity immune memory CD8+ T cells memory homeostasis interleukin-7 interleukin-15 interleukin-7 receptor α proliferation Get full text access Log in, subscribe or purchase for full access. References 1. Masopust, D. ∙ Vezys, V. ∙ Marzo, A.L. ... Preferential localization of effector memory cells in nonlymphoid tissue Science. 2001; 291:2413-2417 2. Jameson, S.C. ∙ Masopust, D. Understanding subset diversity in T cell memory Immunity. 2018; 48:214-226 3. Masopust, D.
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Steady-state, therapeutic, and helminth-induced IL-4 compromise protective CD8 T cell bystander activation

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By Nicholas Joseph Maurice, Talia S Dalzell, Nicholas N Jarjour, Taylor A DePauw
| BioRxiv
Abstract Memory CD8 T cells (Tmem) can be activated into innate-like killers by cytokines like IL-12, IL-15, and/or IL-18; but mechanisms regulating this phenomenon (termed bystander activation) are not fully resolved. We found strain-intrinsic deficiencies in bystander activation using specific pathogen-free mice, whereby basal IL-4 signals antagonize IL-18 sensing. We show that therapeutic and helminth-induced IL-4 impairs protective bystander-mediated responses against pathogens.
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Collaboration between IL-7 and IL-15 enables adaptation of tissue-resident and circulating memory CD8+ T cells

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By Nicholas N Jarjour, Nicholas J. Maurice, Kelsey M. Wanhainen, Talia S Dalzell
| BioRxiv
Abstract Interleukin-7 (IL-7) is considered a critical regulator of memory CD8+ T cell homeostasis, but this is primarily based on analysis of circulating and not tissue-resident memory (TRM) subsets. Furthermore, the cell-intrinsic requirement for IL-7 signaling during memory homeostasis has not been directly tested.
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