Relationship of NKG2C Copy Number with the Distribution of Distinct Cytomegalovirus-Induced Adaptive NK Cell Subsets [INFECTIOUS DISEASE AND HOST RESPONSE]

CD94/NKG2C and lack of FcR (FcR) expression are considered markers of the adaptive NK cell response to human CMV (HCMV) infection. Despite the fact that FcR^– and NKG2C^bright NK cells share some phenotypic, epigenetic, and functional features, their relationship remains unclear. To address this issue, a systematic analysis of NKG2C^bright and FcR expression was carried out in NK cells from a cohort of healthy young adults (n = 81) considering NKG2C copy number, previously related to the magnitude of NKG2C⁺ NK cell expansion. NKG2C^bright and FcR^– NK cells coincided in a subgroup of HCMV⁺ individuals, pointing to a common host–virus interaction pattern. Even though FcR loss was often confined to expanded NKG2C^bright NK cells, both markers appeared occasionally dissociated, consistent with the existence of distinct adaptive NK cell subsets. Remarkably, FcR loss was mostly accumulated within the NKG2C^bright subset in NKG2C^+/+ subjects, whereas NKG2C^–FcR^– NK cell subpopulations were more frequently detected in NKG2C^+/del donors and also in NKG2C^del/del individuals, independently of activating killer Ig–like receptor expression. The distribution of other NK receptors (i.e., killer Ig–like receptor, LILRB1, or CD57) supported a sequential differentiation from NKG2C^brightFcR⁺ to NKG2C^brightFcR^– NK cells. Noticeably, NKG2C^bright NK cells produced more TNF-α in response to Ab-dependent activation, regardless of their FcR levels. Moreover, the TNF-α response of NKG2C^–FcR^– subpopulations was lower than that of concurrent NKG2C^brightFcR^– NK cells, further supporting that FcR levels and enhanced potential for cytokine production are uncoupled. Overall, our data extend the characterization of adaptive NK cell subsets that differentiate in response to HCMV, supporting a relationship between their distribution and NKG2C copy number.

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