消化系恶性肿瘤病人LAK细胞和NK细胞功能与表型的变化

通过观察20例正常人和24例消化系恶性肿瘤病人外周血自然杀伤细胞(NK)和淋巴因子激活的杀伤细胞(LAK)的活性变化,以及加用重组白细胞介素2(rIL-2)刺激前后T淋巴细胞表型变化。结果发现肿瘤病人的NK细胞活性明显下降,但经rIL-2激活后LAK细胞活性得到明显提高,其溶解率接近正常水平。肿瘤病人的总T淋巴细胞(CD_(3+))和辅助/诱导T淋巴细胞(CD_(4+))水平低于正常,但抑制/杀伤淋巴细胞(CD_(8+))水平正常。辅助/诱导淋巴细胞与抑制/杀伤淋巴细胞之比为1.18,低于正常水平(1.55)。经加入rIL-2培养后,CD_(3+)和CD_(8+)淋巴细胞的比率明显升高并达正常水平。而在正常人此变化不明显,且加用rIL-2培养与不加者无显著差异。IL-2受体的表达正常人与肿瘤病人无异。结果显示胃肠道恶性肿瘤病人的免疫机制受到抑制,但能被IL-2提高至正常水平。     

冠心病患者红细胞免疫功能的变化

本文测定了正常人及冠心病患者的红细胞免疫功能。结果表明，冠心病患者的红细胞Ｃ３ｂ受体花环率（ＲＢＣ－Ｃ３ｂＲＲ）降低，红细胞免疫复合物花环率（ＲＢＣ－ＩＣＲ）及循环免疫复合物（ＣＩＣ）增高；且ＣＩＣ与ＲＢＣ－Ｃ３ｂＲＲ呈负相关，与ＲＢＣ－ＩＣＲ呈正相关；ＲＢＣ－Ｃ３ｂＲＲ与ＲＢＣ－ＩＣＲ呈负相关，提示冠心病患者存在红细胞免疫功能低下，可能为继发性改变。     

肺炎支原体感染与过敏性紫癜患儿免疫功能的关系研究

目的探讨肺炎支原体(Mycoplasma pneumoniae,MP)感染与过敏性紫癜患儿免疫功能的关系。方法选择2014年1月至2019年1月期间秦皇岛市第一医院住院及门诊就诊及复诊的过敏性紫癜患儿145例作为研究对象。根据MP-IgM水平将患儿分为MP感染组(MP-IgM≥1:80,)和非MP感染组(MP-IgM<1:80)。采用被动凝集法测定MP-IgM水平,采用流式细胞术测定外周血淋巴细胞亚群(CD3^+、CD4^+、CD8^+、CD19^+、CD16^+56),采用免疫散射比浊法测定免疫球蛋白(IgA、IgM、IgG)和血清补体C3、C4水平,比较两组免疫功能的差异。结果MP感染组CD3^+、CD4^+、CD4^+/CD8^+、CD^+明显低于非MP感染组,CD8^+、CD16^+56明显高于非MP感染组,P<0.05。MP感染组IgA、IgM、IgG、C3、C4水平明显低于非MP感染组,P<0.05。结论MP感染与过敏性紫癜患儿免疫功能具有紧密的关系,其是导致过敏性紫癜患儿免疫功能降低的主要原因之一。     

促红细胞生成素对慢性肾性贫血患者红细胞免疫功能及NK细胞活性的影响

近来 ,我们应用重组人促红细胞生成素 (r Hu E-PO)治疗 1 8例慢性肾功能不全 (CRF)贫血患者 ,并对治疗前后的血红蛋白 (Hb)含量、红细胞 C3 b受体(C3 b R)花环率、红细胞免疫复合物 (IC)花环率及自然杀伤细胞 (NK)活性进行了检测 ,以观察 r Hu EPO对 CRF贫血的疗效 ,探讨 r Hu EPO对红细胞免疫功能及 NK细胞活性的影响。1　资料与方法 :1观察组 :CRF贫血患者 1 8例 ,男 1例、女 7例 ,年龄 1 6～ 5 4岁 ,病程 1～ 1 1年。原发病为慢性肾小球炎 1 2例 ,肾结石 2例 ,狼疮性肾炎、多囊肾、紫癜性肾炎、慢性肾盂炎各 1例。血尿素氮 …     

肺心病患者红细胞免疫功能变化及其临床意义

为探讨红细胞免疫功能在肺心病发病中的作用,我们检测了37例慢性肺心病患者的红细胞免疫功能变化,现报告如下。1 资料与方法1.1 临床资料 本组均根据第二届全国肺心病会议制定的标准诊断。其中男18例,女19例;年龄31～65岁,平均52.2岁。急性加重期19例,缓解期18例。另选择同期健康者35例作为对照组(男19例、女16例,年龄30～64例、平均50.8岁)。     

柯萨奇B组病毒与过敏性紫癜的发病及免疫指标的变化

过敏性紫癜（ＨＳＰ）的发生与多种因素相关，而病毒感染在其中占重要位置。本文通过对２７例ＨＳＰ患儿血清及免疫球蛋白（Ｉｇ）、Ｔ细胞亚群、自然杀伤细胞（ＮＫ）、淋巴因子激活的杀伤细胞（ＬＡＫ）的检测，以探讨ＣＶＢ感染与ＨＳＰ发病的相关性及免疫功能的变化特...     

健康人T细胞及NK细胞活性的随龄性变化

本文系统地观察了不同年龄健康人细胞免疫功能变化。结果表明,T细胞转化及分泌IL-2活性均随增龄下降,且与年龄呈明显相关性(P<0.01),并以60～69岁年龄段活性下降幅度最大。NK细胞毒活性亦在60～69岁年龄段明显下降,但随后变化不大,与年龄无相关性(P>0.05)。本文结果提示,机体在60～69岁时因多种免疫指标产生急剧变化,此时可能是机体老化过程的—个转折点,从预防医学角度看,此时更应注重老年人的保健工作。     

孟鲁司特对过敏性紫癜患儿T细胞亚群变化的影响

目的 探讨孟鲁司特对过敏性紫癜(HSP)患儿T细胞亚群变化的影响.方法 46例HSP患儿随机分成两组,对照组和治疗组分别给予强的松和孟鲁司特治疗1个月.治疗前后采集血样测定T细胞亚群含量.另选21例健康儿童作为正常组.结果 对照组和治疗组总有效率分别为95.6%和91.3%(P>0.05).与正常组比较,治疗组治疗前外周血的CD+4含量和CD+4/CD+8明显下降,CD+8含量明显上升,CD+3变化不明显;治疗组经过治疗后CD+4和CD+4/CD+8明显提高,CD+8降低.结论 孟鲁司特能影响HSP患儿T细胞亚群的含量,对HSP有较好的治疗效果.     

乙型肝炎病毒对自然杀伤细胞免疫活性的影响

目的 了解HBV对NK细胞免疫功能的影响.方法 健康者外周血来源的NK细胞单独培养,或与浆样树突状细胞(pDC)共同培养(NK∶ pDC=5∶1)48 h,加入HepG2.2.15细胞来源的HBV.流式细胞技术测定细胞活性分子的表达,ELISA和细胞内细胞因子染色法(ICS)测定细胞因子含量,检测NK细胞对K562靶细胞的杀伤能力以及NK细胞内穿孔素和颗粒酶的含量以判定NK细胞的杀伤毒性.Wilcoxon符号秩检验进行配对样本分析.结果 HBV对细胞因子(IL-12/IL-18,IL-18/IFNα)活化的NK细胞分泌IFNγ无直接的抑制作用(均P＞0.05).CpG寡脱氧核酸能促进pDC诱导的NK细胞产生IFNγ (1135.4 pg/mL),而HBV对pDC诱导的NK细胞分泌IFNγ具有显著的抑制作用(146.1 pg/mL,P=0.0005).HBV并不影响pDC介导的NK细胞表面活性分子的表达,也不影响pDC介导的NK细胞对K562靶细胞的杀伤毒性以及NK细胞内穿孔素和颗粒酶的含量.结论 HBV并不激活,而是显著抑制pDC诱导的NK细胞分泌IFNγ,从而增加HBV持续感染的可能性.     

PTEN regulates natural killer cell trafficking in vivo

Phosphatase and tensin homolog (PTEN) is a critical negative regulator of the phosphoinositide-3 kinase pathway, members of which play integral roles in natural killer (NK) cell development and function. However, the functions of PTEN in NK cell biology remain unknown. Here, we used an NK cell-specific PTEN-deletion mouse model to define the ramifications of intrinsic NK cell PTEN loss in vivo. In these mice, there was a significant defect in NK cell numbers in the bone marrow and peripheral organs despite increased proliferation and intact peripheral NK cell maturation. Unexpectedly, we observed a significant expansion of peripheral blood NK cells and the premature egress of NK cells from the bone marrow. The altered trafficking of NK cells from peripheral organs into the blood was due to selective hyperresponsiveness to the blood localizing chemokine S1P. To address the importance of this trafficking defect to NK cell immune responses, we investigated the ability of PTEN-deficient NK cells to traffic to a site of tumor challenge. PTEN-deficient NK cells were defective at migrating to distal tumor sites but were more effective at clearing tumors actively introduced into the peripheral blood. Collectively, these data identify PTEN as an essential regulator of NK cell localization in vivo during both homeostasis and malignancy.Natural killer (NK) cells are innate lymphoid cells critical for host defense against pathogens and antitumor responses (1–3). In the naïve mouse, NK cells are distributed among a number of hematopoietic and nonhematopoietic organs, including major reservoirs within the spleen, blood, and bone marrow (BM). Factors that orchestrate NK cell trafficking during homeostasis, including chemokine receptors and adhesion molecules, remain largely unknown. The majority of studies have focused on receptors controlling NK cell migration out of the BM, such as CXCR4 and S1P₅ (4–6). During inflammatory states, other receptors have defined roles for specific tissue homing, including CCR1, CCR5, CXCR3, CX3CR1, and CXCR6 (7). Integrin molecules, such as very late antigen-4 (VLA-4), also have specific functions in retaining NK cells within BM sinusoids (8). However, the downstream intracellular signaling pathways important for trafficking remain unclear, especially in light of the complex interplay of multiple chemotactic signals during an immune response.One family of enzymes regulating a number of chemokine receptors includes the phosphoinositide 3-kinase (PI3K) signaling pathway, which plays a broad role in regulating cellular proliferation, gene expression, survival, cytoskeleton rearrangement, and migration (9). In immune cells, the PI3K pathway may be activated downstream of a number of receptors, including cytokine receptors and G protein-coupled receptors (GPCRs), the latter of which include most chemokine receptors. Stimulation of the PI3Ks results in the generation of phosphatidylinositol phosphate lipids, such as PI(3,4,5)P₃, and subsequent recruitment and activation of downstream signaling proteins, including Vav, Akt, and PDK1 (9, 10). Exogenous inhibition of PI3Ks suppresses perforin and granzyme B polarization and NK cell cytotoxicity (11). Additionally, deficiency of the leukocyte-selective PI3K p110γ or p110δ subunit results in defective NK cell development and maturation and alters the production of IFN gamma (IFN-γ) and cytotoxicity (12–14). New evidence has also linked IL-15 to the mammalian target of rapamycin (mTOR) pathway via PI3K activation (15, 16). Thus, PI3K signaling is a critical pathway for NK cell biological processes.Two primary phosphatases oppose PI3K generation of the active secondary messenger PI(3,4,5)P₃: SH2-containing inositol-5′-phosphatase 1 (SHIP1) and phosphatase and tensin homolog (PTEN). SHIP1 specifically dephosphorylates PI(3,4,5)P₃ to PI(3,4)P₂, whereas PTEN dephosphorylates the 3′ inositol phosphate on PI(3,4,5)P₃, PI(3,4)P₂, and PI(3)P, thereby also counteracting other classes of PI3Ks (10). SHIP1^−/− BM-chimeric mice have no overt alterations in NK cell distribution, and its intrinsic role in NK cell development only affects the terminal differentiation of mature NK cells (17). However, there are no reported studies of PTEN function in NK cells to date. The effects of lymphocyte-selective PTEN deficiency in T and B cells result from increased PI3K signaling and include increased cell survival and proliferation, lowered activation threshold through the B-cell receptor (18), and loss of costimulatory requirements in T cells (19). The role of phosphatases, particularly SHIP1 and PTEN, in cellular migration, however, remains controversial and appears to be dependent on both the cell studied and the mode of stimulation (20–22). Furthermore, unique aspects of PTEN function have been reported, including protein phosphatase activity (23) and regulation via intracellular sequestration to the cytoplasmic membrane (24). As PTEN is a major nonredundant regulator of PI3K signaling, we hypothesized that disruption of PI3K inhibition would uniquely impact NK cell developmental and functional pathways.In this study, we generated NK cell-specific PTEN-deficient mice, which have diminished opposing lipid phosphatase activity to all known PI3K family members. PTEN-deficient mice display significant defects in peripheral organ and BM NK cell compartments, with a large proportion of NK cells being inappropriately localized to the blood. These effects were due in part to alterations in NK cell trafficking in vivo, a defect that also prevented their recruitment to a localized tumor challenge. These results identify a previously unidentified role for PTEN in regulating NK cell tissue distribution during both homeostasis and malignancy in vivo.     

COPD患者红细胞天然免疫粘附功能的测定及意义

目的研究慢性阻塞性肺病(COPD)患者红细胞天然免疫粘附功能情况及意义。方法检测50例COPD及30例正常人红细胞粘附肿瘤细胞的能力,计算结合5个以上红细胞的肿瘤细胞的百分率。结果COPD患者的红细胞天然免疫粘附功能与正常人组相比有显著性差异(P<0.5),COPD的分级与红细胞天然免疫粘附功能密切相关。结论测定COPD患者红细胞天然免疫粘附功能对临床病情判断有一定参考价值。     

A dynamic flux in natural killer cell subsets as a function of the duration of alcohol ingestion

Background: Chronic ethanol (EtOH) consumption is associated with a wide variety of immune abnormalities including changes in T cells, B cells, dendritic cells, and natural killer (NK) cells. However, there is conflicting information as to the direction of such immune changes. The hypothesis that was tested in this report is that, for NK cells, the changes can vary as a function of the duration of alcohol ingestion. Methods: Using the Meadows–Cook murine model of chronic alcohol ingestion, the changes in NK cell function and subset distribution were examined as a function of the duration of alcohol ingestion. Results: Acute alcohol ingestion resulted in decreased number and cytotoxic function of NK cells with no effect on intracellular interferon gamma expression. These abnormalities normalized after 12 to 14 days of alcohol ingestion and there was an increase of NK cell number and cytotoxicity after 8 weeks of continued EtOH ingestion. Ten weeks of continued alcohol consumption results in a significant decrease in the Ly49H+ CD11b+ CD27? splenic NK cell subset; this difference continued to be significant at 30 weeks. Conclusions: This report may explain some of the conflicting data in the literature that examined NK cell activity in alcoholic patients. It is apparent that various abnormalities can be seen in NK cell activity and subset distribution with the flux being a function of the duration of alcohol ingestion. The demonstration of a decrease in the Ly49H+ subset (which is known to be involved in resisting murine cytomegalovirus infection) may explain the reported increase in susceptibility to some viral infections in chronic alcohol abuse. Another novel finding is that changes of some subsets of NK cells are not evident until at least 10 weeks of continued EtOH consumption.     

原发性肺自然杀伤/T细胞淋巴瘤二例临床分析

目的 提高对原发性肺自然杀伤(natural killer,NK)/T细胞淋巴瘤的诊断和鉴别.方法 报道2006年我院收治的2例原发性肺NK/T细胞淋巴瘤患者,复习国内外文献报道的3例患者临床及实验室检查特征.结果 患者临床表现为发热、咳嗽、呼吸困难等,抗生素治疗无效.胸部影像学表现为单发或多发的团块状、斑片状实变影,可出现单侧或双侧胸腔积液(4/5),无肺门和纵隔淋巴结肿大.多数患者(3/5)EB病毒(+).肺组织活检病理学表现为大量异常淋巴细胞浸润,肿瘤细胞呈血管中心性生长,并伴有明显的组织坏死和血管破坏;肿瘤细胞免疫表型为CD56(+)、CD3(+),穿孔素(+)、T淋巴细胞胞质内抗原-1(+)和(或)颗粒酶(+),CD20(-).大部分患者(4/5)在半年内由于呼吸衰竭死亡.结论 原发性肺NK/T细胞淋巴瘤罕见,且临床表现为发热伴肺部阴影且疑诊肺炎的患者,若同时合并白细胞减少伴乳酸脱氢酶明显升高,在鉴别诊断时应考虑原发性肺NK/T细胞淋巴瘤.     

白细胞介素-23对炎症性肠病患者外周血自然杀伤细胞的免疫调节作用

目的 研究白细胞介素(IL)-23对炎症性肠病(IBD)患者外周血中自然杀伤(NK)细胞促炎细胞因子分泌和细胞毒作用的影响,探讨其在IBD发病中的意义.方法 利用免疫磁珠分离12名健康人、16例克罗恩病(CD)患者和25例溃疡性结肠炎(UC)患者外周血NK细胞.体外培养NK细胞,并予空白刺激、IL-23刺激、IgG刺激或IL-23+IgG联合刺激.酶联免疫吸附试验法检测细胞培养上清中肿瘤坏死因子(TNF)-αa和干扰素(IFN)-γ分泌水平.流式细胞仪检测经不同刺激培养的NK细胞对K562细胞的细胞毒作用.结果 正常对照组的NK细胞经人IgG和IL-23单独刺激后TNF-α、IFN-γ的分泌水平未明显增高(P值均＞0.05),二者联合刺激则能显著促进TNF-α、IFN-γ分泌(P值均＜0.05).单独应用IgG刺激CD和UC患者NK细胞分泌TNF-α、IFN-γ的效果不明显(P值均＞0.05).单独应用IL-23则具刺激作用(P值均＜0.05),二者联合应用的刺激作用更明显(P值均＜0.01).IL-23单独刺激和联合刺激均不能增强正常对照组NK细胞的细胞毒作用(P值均＞0.05).但单独应用IL-23可增强UC和CD患者NK细胞的细胞毒作用(分别为51.5%±7.1%和50.2%±8.7%,P值均＜0.05),且联合刺激可进一步增强该作用(分别为65.3%±6.6%和62.4%±5.5%,P值均＜0.01).结论 IL-23能刺激IBD患者NK细胞分泌TNF-α和IFN-γ,并能增强NK细胞的细胞毒作用,可能直接参与了IBD的发病过程.     

肺结核合并糖尿病患者自然杀伤T细胞的变化特点

目的 研究肺结核合并糖尿病患者自然杀伤T细胞(NKT细胞)的临床变化特点.方法 2008年1月至2010年6月,选取上海市肺科医院住院的肺结核患者40例为肺结核组,其中男26例,女14例,年龄19～65岁,平均(42±11)岁,平均体重指数(20.6±4.7)kg/m2;肺结核合并糖尿病患者40例为合并糖尿病组,其中男25例,女15例,年龄34～68岁,平均(47±10)岁,平均体重指数(21.3±1.9)kg/m2,采用流式细胞术检测外周血和BALF中表型为T细胞受体Vα24+Vβ11+的NKT细胞数量.同期选取门诊体检志愿者37例为对照组,其中男25例,女12例,年龄21～60岁,平均(42±12)岁,平均体重指数(21.9±5.4)kg/m2;门诊糖尿病患者38例为糖尿病组,其中男23例,女15例,年龄36～65岁,平均(44±8)岁,平均体重指数(20.5±3.2)kg/m2,检测外周血NKT细胞的数量[中位数(四分位间距)].计数资料比较采用t检验,组间两两比较采用SNK和LSD检验,采用双变量进行相关性分析.结果 肺结核组外周血NKT细胞[1.1%(0.8%～1.3%)]和合并糖尿病组[0.8%(0.5%～1.0%)]均明显高于对照组[0.4%(0.3%～0.7%)]和糖尿病组[0.3%(0.2%～0.5%)],均差异有统计学意义(q值为3.258～7.074,均P＜0.01);肺结核组与合并糖尿病组比较,差异有统计学意义(q=2.827,P＜0.01).肺结核组BALF中NKT细胞数[0.7%(0.3%～1.0%)]明显高于合并糖尿病组[0.3%(0.2%～0.6%)],差异有统计学意义(t=2.394,P＜0.05).BALF和外周血的NKT细胞数在轻度[0.9%(0.3%～1.3%)和1.0%(0.8%～1.3%)]、中度[0.4%(0.3%～0.9%)和1.0%(0.8%～1.3%)]和重度肺结核患者[0.3%(0.3%～0.5%)和0.7%(0.5%～1.1%)]中的分布差异均有统计学意义(F值分别为4.535和3.763,均P＜0.05),病情越重NKT细胞数越低.外周血与BALF中NKT细胞数量呈正相关(r=0.709,P＜0.01).结论 NKT细胞在抗MTB感染中发挥着重要作用.肺结核合并糖尿病患者体内复杂的微环境影响NKT细胞发挥其功能,使其保护性免疫力降低.

Abstract：

Objective To investigate the changes of NKT cells in pulmonary tuberculosis patients ( PTB ) complicated by diabetes mellitus ( DM ). Methods From January 2008 to June 2010, 40 cases of PTB patients without DM hospitalized in Shanghai Pulmonary Hospital were selected. There were 26 males and 14 females, aged from 19 -65 ( mean, 42 ± 11 ) years, with an average BMI ( 20.6 ±4.7 ) kg/m2.Forty cases of PTB complicated with DM were included as patient controls which consisted of 25 males and 15 females, aged from 34 -68 ( mean, 47 ± 10 )years, with an average BMI ( 21.3 ± 1.9 ) kg/m2. Thirtyseven healthy controls and 38 cases of non-TB DM in the outpatient department for physical examination were enrolled at the same period. There were 25 male and 12 female healthy controls, aged from 21 -60 ( mean,42 ± 12 ) years, with an average BMI ( 21.9 ±5.4 ) kg/m2. There were 23 males and 15 females in the nonTB DM volunteers, aged from 36 -65 ( mean, 44 ±8 ) years, with an average BMI ( 20. 5 ±3. 2 ) kg/m2.The percentages of NKT cells with the phenotype of TCRVα.24 + Vβ11 + in peripheral blood and bronchial alveolar lavage fluid ( BALF ) were tested by flow cytometry for all the patients. Continuous data were analyzed by t test. Multiple comparisons were performed by SNK and LSD test. Results The percentages of NKT cells in peripheral blood from non-diabetic PTB [ 1.1%( 0. 8% - 1.3% ) ] and diabetic PTB patients [0. 8% (0. 5% - 1.0% ) ] were all significantly higher as compared with healthy controls [0. 4% (0. 3% -0. 7% ) ] and DM patients without TB [ 0. 3% ( 0. 2% - 0. 5% ) ] ( q = 3. 258 - 7. 074, respectively, all P＜0. 01 ). The percentages of NKT cells in peripheral blood from non-diabetic PTB patients were also significantly higher as compared with diabetic PTB patients ( q = 2. 827, P ＜ 0. 01 ). The percentages of NKT cells in BALF from non-diabetic PTB patients [0. 7% (0. 3% - 1. 0% ) ] were significantly higher as compared with diabetic PTB patients [ 0. 3% ( 0. 2% - 0. 6% ) ] ( t = 2. 394, P ＜ 0. 05 ). The percentages of NKT cells from BALF in mild, moderate and severe PTB patients were [0. 9% (0. 3% - 1.3% ) ], [0. 4% (0. 3% -0. 9% ) ] and [0. 3% (0. 3% - 0. 5% ) ], respectively, which were significantly different ( F= 4. 535, P ＜0. 05 ). The percentages of NKT cells from peripheral blood in mild, moderate and severe PTB patients were[1.0%(0.8% -1.3%)], [1.0%(0.8% -1.3%)] and [0.7% (0.5% -1.1%)], respectively, which were also significantly different (F =3. 763, P ＜0. 05). The percentages of NKT cells from peripheral blood had a positive correlation with those from BALF ( r = 0. 709, P ＜ 0. 01 ). Conclusions NKT cells play an important role in TB infection. The complicated milieus in PTB patients with DM have adverse effects on NKT cells, resulting in their dysfunction.     

恒定的自然杀伤T淋巴细胞在肝脏抗肿瘤免疫中的作用与机制

恒定的自然杀伤T淋巴细胞(iNKT细胞)是来源于胸腺的T淋巴细胞亚群,同时表达自然杀伤细胞相关受体和T淋巴细胞受体。iNKT细胞广泛分布于全身,在肝脏内富集,表现出独特的功能特性,可以分泌细胞因子并调节微环境其他免疫细胞活性,以达到免疫监视及预防疾病的作用,尤其是在肿瘤微环境中,iNKT细胞能够激发肝脏抗肿瘤免疫反应、逆转免疫抑制微环境状态。就iNKT细胞的生物学特性及其在肝脏免疫稳态中的特殊作用,尤其就iNKT细胞的抗肿瘤作用与机制作一综述。     

HBV感染对肝脏自然杀伤细胞和固有淋巴样细胞22的影响

目的探讨HBV感染对肝脏自然杀伤细胞(NK细胞)和固有淋巴样细胞(ILC)22的影响,为阐明HBV感染诱导机体固有免疫应答的机制提供理论和实验依据。方法选取6~8周龄雄性BALB/c小鼠10只,随机分为实验组和对照组,每组各5只。实验组小鼠经尾静脉高压注射含10μg HBV全基因组质粒的生理盐水(体积相当于9%小鼠体质量);对照组小鼠仅注射生理盐水。4 d后处死小鼠,分离肝脏内淋巴细胞,应用流式细胞术检测肝脏内淋巴细胞中NK细胞亚群和ILC22细胞亚群的比例。组间比较采用t检验。结果高压尾静脉注射HBV全基因组质粒可诱导小鼠产生高水平的HBs Ag和HBe Ag,伴有血清ALT水平升高。实验组小鼠肝脏内NK细胞的比例较对照组小鼠显著升高[(25.90±4.92)%vs(12.98±2.13)%,t=3.811,P=0.003],但CD127+NK细胞和CD127-NK细胞亚群在NK细胞中所占比例在2组之间差异均无统计学意义(P值均0.05)。实验组小鼠肝脏内NKp46+ILC22细胞亚群比例较对照组明显升高[(36.05±6.85)%vs(10.22±3.54)%,t=7.372,P0.001],但NKp46-ILC22细胞亚群的比例在2组之间差异无统计学意义(P0.05)。结论 HBV感染可诱导肝脏内NK细胞和NKp46+ILC22水平升高,从而促进肝脏固有免疫应答。