Journal
IMMUNITY
Volume 37, Issue 3, Pages 549-562Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2012.05.029
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Funding
- Albert Einstein College of Medicine of Yeshiva University
- National Institute of Health [R21AI095835]
- Agence Nationale pour la Recherche [ANR-10-LABX-61]
- InCa Atip/Avenir
- fundation Bettencourt-Schueller
- Albert Einstein Cancer Center (NCI) [2P30CA013330]
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Memory CD8(+) T cells induced upon immunization exhibit improved functional features that contribute to protection of immunized hosts. Although both cognate antigen recognition and inflammation are important for memory CD8(+) T cell reactivation, the relative contribution of these factors and the cell types providing these signals in vivo are poorly defined. Here, we show that Ly6C(+)CCR2(+) inflammatory monocytes, a subset of monocytes, largely orchestrate memory CD8(+) T and NK lymphocytes activation by differentiating into interleukin-18 (IL-18)- and IL-15-producing cells in an inflammasome and type I interferon-IRF3-dependent manner. Memory CD8(+) T cells became potent effector cells by sensing inflammation from monocytes independently of their cognate antigen. Like NK cells, they underwent rapid mobilization, upregulated intense and sustained effector functions during bacterial, viral, and parasitic infections, and contributed to innate responses and protection in vivo. Thus, inflammatory monocyte-derived IL-18 and IL-15 are critical to initiate memory CD8(+) T and NK lymphocytes differentiation into antimicrobial effector cells.
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