Abstract
The aim of this study was to characterize NK (CD56+CD3−) and NKT-like cell (CD56+CD3+) responses early after chikungunya infection. Expression profiling and functional analysis of T/NK/NKT-like cells were performed on samples from 56 acute and 31 convalescent chikungunya patients and 56 control individuals. The percentages of NK cells were high in both patient groups, whereas NKT-like cell percentages were high only in the convalescent group. The percentages of NKp30+CD3−CD56+, NKp30+CD3+CD56+, CD244+CD3−CD56+, and CD244+CD3+CD56+cells were high, whereas the percentages of NKG2D+CD3−CD56+ and NKG2D+CD3+CD56+cells were low in both patient groups. The percentages of NKp44+CD3−CD56+ cells were high in both patient groups, whereas the percentages of NKp44+CD3+CD56+ cells were higher in the acute group than in convalescent and control groups. The percentages of NKp46+CD3−CD56+ cells were high in both patient groups. Higher percentages of perforin+CD3−CD56+ and perforin+CD3+CD56+ cells were observed in acute and convalescent patients, respectively. Higher cytotoxic activity was observed in acute patients than in controls. IFN-γ expression on NK cells of convalescent patients and on NKT-like cells of both patient groups was indicative of the regulatory role of NK and NKT-like cells. Collectively, these data showed that higher expression of activating receptors on NK/NKT-like cells and perforin+ NK cells in acute patients could be responsible for increased cytotoxicity. The observed expression of perforin+ NK cells in the acute phase and IFN-γ+ NKT-like cells in the subsequent convalescent stage showed that NK/NKT-like cells mount an early and efficient response to chikungunya virus. Further study of the molecular mechanisms that limit viral dissemination/establishment of chronic disease will aid in understanding how NK/NKT-like cells control chikungunya infection.
Highlights
Chikungunya (CHIK), a mosquito-borne viral disease caused by the chikungunya virus (CHIKV), has caused global concern since its re-emergence in several Asian and African countries (Powers and Logue, 2007)
Natural killer (NK) (CD56+CD3−) and natural killer T (NKT)-like Cell (CD56+CD3+) Subsets in CHIK Patients To evaluate the impact of CHIKV infection on the phenotype of innate immune cells, the percentages of NK and NKT-like cells from acute and convalescent patients were assessed using flow cytometry
NK Cell Receptor (NKR) Expression on NK Cells from CHIK Patients we investigated whether the increased NK cell percentages were related to changes in expression of activation and inhibitory receptors
Summary
Chikungunya (CHIK), a mosquito-borne viral disease caused by the chikungunya virus (CHIKV), has caused global concern since its re-emergence in several Asian and African countries (Powers and Logue, 2007). The functional activity of NK/NKTlike cells is regulated through their repertoire of activation (NKG2C, NKG2D, NKp30, NKp44, and NKp46) and inhibitory (CD158a, CD158b, KIR3DL1, and NKG2A) receptors, which recognize ligands on the surface of target cells (Peralbo et al, 2007; Watzl and Long, 2010; Das and Tripathy, 2014) Upon activation, both NK and NKT-like cells produce inflammatory cytokines, such as IFN-γ, and lyse target cells by exocytosis of perforin and granzyme, leading to inhibition of viral replication and enhancement of cytotoxicity against target cells (Biron and Brossay, 2001; Janeway and Medzhitov, 2002; Peralbo et al, 2007; Das and Tripathy, 2014). NK cells contribution toward arthritis in the Ross River virus infection has been reported by Aaskov et al (1987)
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