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

Autor(es)

Belizario, Jose E. ^[1] ; Neyra, Jennifer M. ^[1] ; Setubal Destro Rodrigues, Maria Fernanda ^[2]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Dept Pharmacol, Sao Paulo - Brazil

^[2] Nove Julho Univ, Biophoton Appl Hlth Sci, Sao Paulo - Brazil

• Tipo de documento: Artigo de Revisão
• Fonte: Innate Immunity; v. 24, n. 8, p. 452-465, NOV 2018.
• Citações Web of Science: 0

Resumo

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)

• Processo FAPESP: 18/11053-1 - 2018 NCRI Cancer Conference - National Cancer Research Institute Cancer Conference
• Beneficiário: Maria Fernanda Setúbal Destro Rodrigues
• Modalidade de apoio: Auxílio à Pesquisa - Reunião - Exterior
• Processo FAPESP: 14/12658-3 - Efeito do tratamento com cetuximab em células-tronco tumorais de carcinoma epidermóide bucal
• Beneficiário: Maria Fernanda Setúbal Destro Rodrigues
• Modalidade de apoio: Bolsas no Exterior - Estágio de Pesquisa - Pós-Doutorado