中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
CHINESE JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY
2015年
3期
161-165,166
,共6页
梁华%贾曼雪%李丹%邵一鸣
樑華%賈曼雪%李丹%邵一鳴
량화%가만설%리단%소일명
人类免疫缺陷病毒%CD56+T细胞%表型%细胞毒效应
人類免疫缺陷病毒%CD56+T細胞%錶型%細胞毒效應
인류면역결함병독%CD56+T세포%표형%세포독효응
Human immunodeficiency virus%CD56+T cells%Phenotype%Cytotoxicity
目的:探讨HIV-1早期感染者外周血中CD56+T细胞表型和功能变化特点,了解该变化与疾病进展状态的相关性。方法采集HIV-1早期感染者样品53例,HIV-1阴性健康对照31例,分离外周血单个核细胞( PBMC )后,流式细胞术检测 CD56+T 细胞数量及细胞表面分子 CD16、CD161、NKB1、NKG2A、NKp46、NKG2D、NKG2C、CD158a表达水平。将PBMC与K562细胞共孵育,检测CD56+T细胞分泌细胞因子IFN-γ和TNF-α的水平,以及细胞毒效应分子CD107a的水平。结果HIV-1早期感染者外周血中CD56+T细胞数量较健康对照明显减少(P=0.025),且与血浆病毒载量呈负相关(P=0.021,r=-0.316)。 CD56+T细胞表面分子CD16(P=0.003)、CD161(P=0.023)、NKB1(P=0.023)、NKp46(P=0.021)表达较健康对照显著降低,其中NKB1的表达水平与CD4+T细胞数量呈正相关(P=0.007,r=0.364),而与病毒载量呈负相关(P=0.030,r=-0.299)。 HIV-1早期感染者CD56+T细胞自发分泌IFN-γ和TNF-α以及细胞毒效应分子CD107a水平明显低于健康对照( P均<0.001),在靶细胞K562存在情况下,其杀伤能力也显著低于健康对照( IFN-γ和TNF-α:P均<0.001,CD107a:P=0.016)。结论 HIV-1早期感染者CD56+T细胞数量下降,表型发生改变,分泌细胞因子和细胞毒效应分子能力下降,提示在HIV-1感染早期CD56+T细胞即受到损伤,且与疾病进展相关。
目的:探討HIV-1早期感染者外週血中CD56+T細胞錶型和功能變化特點,瞭解該變化與疾病進展狀態的相關性。方法採集HIV-1早期感染者樣品53例,HIV-1陰性健康對照31例,分離外週血單箇覈細胞( PBMC )後,流式細胞術檢測 CD56+T 細胞數量及細胞錶麵分子 CD16、CD161、NKB1、NKG2A、NKp46、NKG2D、NKG2C、CD158a錶達水平。將PBMC與K562細胞共孵育,檢測CD56+T細胞分泌細胞因子IFN-γ和TNF-α的水平,以及細胞毒效應分子CD107a的水平。結果HIV-1早期感染者外週血中CD56+T細胞數量較健康對照明顯減少(P=0.025),且與血漿病毒載量呈負相關(P=0.021,r=-0.316)。 CD56+T細胞錶麵分子CD16(P=0.003)、CD161(P=0.023)、NKB1(P=0.023)、NKp46(P=0.021)錶達較健康對照顯著降低,其中NKB1的錶達水平與CD4+T細胞數量呈正相關(P=0.007,r=0.364),而與病毒載量呈負相關(P=0.030,r=-0.299)。 HIV-1早期感染者CD56+T細胞自髮分泌IFN-γ和TNF-α以及細胞毒效應分子CD107a水平明顯低于健康對照( P均<0.001),在靶細胞K562存在情況下,其殺傷能力也顯著低于健康對照( IFN-γ和TNF-α:P均<0.001,CD107a:P=0.016)。結論 HIV-1早期感染者CD56+T細胞數量下降,錶型髮生改變,分泌細胞因子和細胞毒效應分子能力下降,提示在HIV-1感染早期CD56+T細胞即受到損傷,且與疾病進展相關。
목적:탐토HIV-1조기감염자외주혈중CD56+T세포표형화공능변화특점,료해해변화여질병진전상태적상관성。방법채집HIV-1조기감염자양품53례,HIV-1음성건강대조31례,분리외주혈단개핵세포( PBMC )후,류식세포술검측 CD56+T 세포수량급세포표면분자 CD16、CD161、NKB1、NKG2A、NKp46、NKG2D、NKG2C、CD158a표체수평。장PBMC여K562세포공부육,검측CD56+T세포분비세포인자IFN-γ화TNF-α적수평,이급세포독효응분자CD107a적수평。결과HIV-1조기감염자외주혈중CD56+T세포수량교건강대조명현감소(P=0.025),차여혈장병독재량정부상관(P=0.021,r=-0.316)。 CD56+T세포표면분자CD16(P=0.003)、CD161(P=0.023)、NKB1(P=0.023)、NKp46(P=0.021)표체교건강대조현저강저,기중NKB1적표체수평여CD4+T세포수량정정상관(P=0.007,r=0.364),이여병독재량정부상관(P=0.030,r=-0.299)。 HIV-1조기감염자CD56+T세포자발분비IFN-γ화TNF-α이급세포독효응분자CD107a수평명현저우건강대조( P균<0.001),재파세포K562존재정황하,기살상능력야현저저우건강대조( IFN-γ화TNF-α:P균<0.001,CD107a:P=0.016)。결론 HIV-1조기감염자CD56+T세포수량하강,표형발생개변,분비세포인자화세포독효응분자능력하강,제시재HIV-1감염조기CD56+T세포즉수도손상,차여질병진전상관。
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-γand TNF-αreleased 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).Sponta-neous secretion of IFN-γand TNF-αby CD56+T cells and the expression of CD107a were dramatically in-hibited 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 prima-ry 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-γand 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 cy-tokines and cytotoxic molecular were also detected, indicating the dysfunction of CD56+T cells appeared dur-ing early stage of HIV-1 infection and was associated with disease progression.