## Abstract 4β1BBL^β/β^ mice have a defect in recall CD8^+^ T cell responses to viruses, whereas CD4^+^ T cell responses to virus are unimpaired in these mice. In contrast, both CD4^+^ and CD8^+^ T cells respond to 4β1BB ligand (4β1BBL) __in vitro__. To clarify the role of 4β1BB/4β1BBL in CD4^+^ ve
Biphasic role of 4-1BB in the regulation of mouse cytomegalovirus-specific CD8+ T cells
β Scribed by Ian R. Humphreys; Seung-Woo Lee; Morgan Jones; Andrea Loewendorf; Emma Gostick; David A. Price; Chris A. Benedict; Carl F. Ware; Michael Croft
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 296 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0014-2980
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β¦ Synopsis
Abstract
The initial requirement for the emergence of CMVβspecific CD8^+^ T cells is poorly understood. Mice deficient in the cosignaling TNF superfamily member, 4β1BB, surprisingly developed exaggerated early CD8^+^ Tβcell responses to mouse CMV (MCMV). CD8^+^ T cells directed against acute MCMV epitopes were enhanced, demonstrating that 4β1BB naturally antagonizes these primary populations. Paradoxically, 4β1BBβdeficient mice displayed reduced accumulation of memory CD8^+^ T cells that expand during chronic/latent infection. Importantly, the canonical TNFβrelated ligand, 4β1BBL, promoted the accumulation of these memory CD8^+^ T cells, whereas suppression of acute CD8^+^ T cells was independent of 4β1BBL. These data highlight the dual nature of the 4β1BB/4β1BBL system in mediating both stimulatory and inhibitory cosignaling activities during the generation of antiβMCMV immunity.
π SIMILAR VOLUMES
## Abstract CD8^+^ T cells are critical for protecting the body from infectious disease. To achieve this protection, CD8^+^ T cells must undergo a highly involved process of differentiation that involves the activation of naΓ―ve/quiescent cells followed by robust rounds of cell division and the acqu