The biology of natural killer cells during sepsis.

Publisher: Blackwell Scientific Publications Country of Publication: England NLM ID: 0374672 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2567 (Electronic) Linking ISSN: 00192805 NLM ISO Abbreviation: Immunology Subsets: MEDLINE

Original Publication: Oxford : Blackwell Scientific Publications

Lymphocyte Activation*; Bacterial Infections/*immunology ; Interferon-gamma/*immunology ; Killer Cells, Natural/*immunology ; Sepsis/*immunology; Animals ; Bacterial Infections/pathology ; Bacterial Infections/therapy ; Humans ; Killer Cells, Natural/pathology ; Mice ; Sepsis/pathology ; Sepsis/therapy

Natural killer (NK) cells are large granular lymphocytes largely recognized for their importance in tumour surveillance and the host response to viral infections. However, as the major innate lymphocyte population, NK cells also coordinate early responses to bacterial infections by amplifying the antimicrobial functions of myeloid cells, especially macrophages, by production of interferon-γ (IFN-γ). Alternatively, excessive NK cell activation and IFN-γ production can amplify the systemic inflammatory response during sepsis resulting in increased physiological dysfunction and organ injury. Our understanding of NK cell biology during bacterial infections and sepsis is mostly derived from studies performed in mice. Human studies have demonstrated a correlation between altered NK cell functions and outcomes during sepsis. However, mechanistic understanding of NK cell function during human sepsis is limited. In this review, we will review the current understanding of NK cell biology during sepsis and discuss the challenges associated with modulating NK cell function during sepsis for therapeutic benefit.
(© 2017 John Wiley & Sons Ltd.)

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R01 GM066885 United States GM NIGMS NIH HHS; R01 GM121711 United States GM NIGMS NIH HHS

Keywords: inflammation; innate lymphoid cells; natural killer cell; sepsis

0 (IFNG protein, human)
82115-62-6 (Interferon-gamma)

Date Created: 20171025 Date Completed: 20180813 Latest Revision: 20190201

20240628

PMC5765373

10.1111/imm.12854

29064085