Analysis of the phenotypes and the function of CD56+ T cells during primary HIV-1 infection

Abstract

Objective To investigate the changes of phenotypes and function of CD56+ T cells during primary HIV-1 infection and their relationship with disease progression. Methods Peripheral blood mononuclear cells (PBMCs) were collected from 53 subjects with primary HIV-1 infection and 31 HIV-1-negative healthy subjects. The percentages of CD56+ T cells and the expression of several phenotypic markers on CD56+ T cells including CD16, CD161, NKB1, NKG2A, NKp46, NKG2D, NKG2C and CD158a were analyzed by flow cytometry. IFN-γ and TNF-α released by CD56+ T cells with and without K562 stimulation and the levels of cytotoxic molecular CD107a were measured. Results The percentages of CD56+ T cells in patients with primary HIV-1 infection were significantly lower than those of healthy subjects (P=0.025). The levels of CD56+ T cells were negatively related to the viral loads in plasma samples (P=0.021, r=-0.316). Compared with healthy subjects, the expression of CD16 (P=0.003), CD161 (P=0.023), NKB1 (P=0.023) and NKp46 (P=0.021) on CD56+ T cells were decreased in patients with primary HIV-1 infection. The levels of NKB1 were positively related to the CD4+ T cell counts (P=0.007, r=0.364), but were negatively related to the viral loads in plasma samples (P=0.030, r=-0.299). Spontaneous secretion of IFN-γ and TNF-α by CD56+ T cells and the expression of CD107a were dramatically inhibited in patients with primary HIV-1 infection as compared with healthy subjects (all P<0.001). Moreover, the killing ability of CD56+ T cells against K562 target cells was weakened in patients with primary HIV-1 infection as the levels of IFN-γ-, TNF-α- and CD107a-producting CD56+ T cells were significantly decreased (P<0.001 for IFN-γ and TNF-α, P=0.016 for CD107a). Conclusion Inhibited expression and altered phenotypes of CD56+ T cells were identified during primary HIV-1 infection. Lower levels of cytokines and cytotoxic molecular were also detected, indicating the dysfunction of CD56+ T cells appeared during early stage of HIV-1 infection and was associated with disease progression. Key words: Human immunodeficiency virus; CD56+ T cells; Phenotype; Cytotoxicity