PMC:7200337 / 24452-27804 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7200337","sourcedb":"PMC","sourceid":"7200337","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7200337","text":"Impairment of NK Cell Function in SARS-CoV-2 Infection\nEx vivo NK cells from peripheral blood of COVID-19 patients have reduced intracellular expression of CD107a, Ksp37, granzyme B, and granulysin, suggesting an impaired cytotoxicity, as well as an impaired production of chemokines, IFN-ɣ, and TNF-α (Wilk et al., 2020, Zheng et al., 2020b). Several pathways may contribute to the dysregulation of NK cells. While influenza virus infects NK cells and induces apoptosis (Mao et al., 2009), lung NK cells do not express the entry receptor for SARS-CoV-2, ACE2, and are therefore unlikely to be directly infected by SARS-CoV-2 (Travaglini et al., 2020). The majority of NK cells found in human lung display a mature CD16+KIR+CD56dim phenotype and are able to induce cell cytotoxicity in response to loss of human leukocyte antigen (HLA) class I or through Fc receptor signaling, although to a lower extent than their peripheral blood counterpart (Marquardt et al., 2017). Killer-immunoglobulin receptors (KIRs) are acquired during NK cell development alongside CD16 (FcRγIIIA) and are essential for NK cell licensing and subsequent capacity for cytolytic function (Sivori et al., 2019). Frequencies of NK cells expressing CD16 and/or KIRs are decreased in the blood following SARS-CoV-2 and SARS-CoV-1 infection, respectively (Xia et al., 2004, Wang et al., 2020d). Collectively, the data suggest either an impaired maturation of the NK compartment or migration of the mature, circulating NK cells into the lungs or other peripheral tissues of SARS-CoV-2-infected patients.\nThe immune checkpoint NKG2A is increased on NK cells and CD8 T cells from COVID-19 patients (Zheng et al., 2020b). NKG2A inhibits cell cytotoxicity by binding the non-classical HLA-E molecule (Braud et al., 1998, Brooks et al., 1997), and this interaction is strongly correlated with poor control of HIV-1 infection (Ramsuran et al., 2018). Genes encoding the inhibitory receptors LAG3 and TIM3 are also upregulated in NK cells from COVID-19 patients (Wilk et al., 2020, Hadjadj et al., 2020). Thus, increased immune checkpoints on NK cells might contribute to viral escape. Additionally, COVID-19 patients have higher plasma concentrations of IL-6 (Huang et al., 2020b), which significantly correlate with lower NK cell numbers (Wang et al., 2020d, Wang et al., 2020f). In vitro stimulation by IL-6 and soluble IL-6 receptor has previously revealed impaired cytolytic functions (perforin and granzyme B production) by healthy donor NK cells, which can be restored following addition of tocilizumab (IL-6R blockade) (Cifaldi et al., 2015). TNF-α is also upregulated in the plasma of COVID-19 patients (Huang et al., 2020b), and ligand-receptor interaction analysis of peripheral blood scRNA-seq data suggests that monocyte-secreted TNF-α might bind to its receptors on NK cells (Guo et al., 2020). TNF-α is known to contribute to NK cell differentiation (Lee et al., 2009), which includes downregulation of NKp46 (Ivagnès et al., 2017), though no effect of TNF-α or IL-6 on NK cell-mediated ADCC has been reported so far. Collectively, these data suggest that crosstalk with monocytes might impair NK cell recognition and killing of SARS-CoV-2-infected cells, and antibodies targeting IL-6 and TNF-signaling may benefit enhanced NK cell functions in COVID-19 patients 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