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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

When and how NK cell-induced programmed cell death benefits immunological protection against intracellular pathogen infection

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Author(s):
Belizario, Jose E. [1] ; Neyra, Jennifer M. [1] ; Setubal Destro Rodrigues, Maria Fernanda [2]
Total Authors: 3
Affiliation:
[1] Univ Sao Paulo, Dept Pharmacol, Sao Paulo - Brazil
[2] Nove Julho Univ, Biophoton Appl Hlth Sci, Sao Paulo - Brazil
Total Affiliations: 2
Document type: Review article
Source: Innate Immunity; v. 24, n. 8, p. 452-465, NOV 2018.
Web of Science Citations: 0
Abstract

NK cells are innate lymphoid cells that exert a key role in immune surveillance through the recognition and elimination of transformed cells and viral, bacterial, and protozoan pathogen-infected cells without prior sensitization. Elucidating when and how NK cell-induced intracellular microbial cell death functions in the resolution of infection and host inflammation has been an important topic of investigation. NK cell activation requires the engagement of specific activating, co-stimulatory, and inhibitory receptors which control positively and negatively their differentiation, memory, and exhaustion. NK cells secrete diverse cytokines, including IFN-gamma, TNF-alpha/beta, CD95/FasL, and TRAIL, as well as cytoplasmic cytotoxic granules containing perforin, granulysin, and granzymes A and B. Paradoxically, NK cells also kill other immune cells like macrophages, dendritic cells, and hyper-activated T cells, thus turning off self-immune reactions. Here we first provide an overview of NK cell biology, and then we describe and discuss the life-death signals that connect the microbial pathogen sensors to the inflammasomes and finally to cell death signaling pathways. We focus on caspase-mediated cell death by apoptosis and pro-inflammatory and non-caspase-mediated cell death by necroptosis, as well as inflammasome- and caspase-mediated pyroptosis. (AU)

FAPESP's process: 18/11053-1 - 2018 NCRI cancer conference - national cancer research institute cancer conference
Grantee:Maria Fernanda Setúbal Destro Rodrigues
Support type: Research Grants - Meeting - Abroad
FAPESP's process: 14/12658-3 - Effects of cetuximab treatment in the behaviour of cancer stem cell in oral squamous cell carcinoma
Grantee:Maria Fernanda Setúbal Destro Rodrigues
Support type: Scholarships abroad - Research Internship - Post-doctor