组织相容性抗原CD45RO肿瘤坏死因子在桥本氏甲状腺炎和亚急性甲状腺炎的表达与免疫损伤的关系及临床意义

目的 :探讨活化T淋巴细胞、肿瘤坏死因子 -α(TNF -α)、组织相容性抗原 (HLA—DR)在桥本氏甲状腺炎 (HT)和亚急性甲状腺炎 (SAT)发病过程中的作用 ,为深入对两病的免疫损伤机理、临床治疗的认识提供理论依据。方法 :应用组织化学、免疫组织化学技术 (S -P法 ) ,观察活化T淋巴细胞标志CD4 5RO、TNF -α、HLA—DR的单克隆抗体在 4 3例HT和 4 2例SAT患者甲状腺组织中的表达。结果 :除正常甲状腺外 ,各例标本浸润的单个核细胞 (TG—MNC)均呈现不同程度的单抗阳性染色。在HT和SAT中 :①CD4 5RO、HLA—DR在其TG—MNC阳性率表达上HT高于SAT ,有显著差异 (0 0 1

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桥本甲状腺炎甲状腺组织中共刺激分子的表达

目的:探讨共刺激分子在桥本甲状腺炎(HT)发病中的免疫病理作用。方法:采用免疫组织化学法检测20例HT和20例甲状腺瘤旁正常组织(对照组)CD40/CD40L、B7-1/CD28、GL50、CD4和CD8分子的表达,进行分析。结果:(1)HT甲状腺滤泡细胞(TFC)B7-1表达明显高于对照组,CD40表达明显低于对照组,且有显著性差异(P<0.01);(2)HT组织浸润细胞CD28、GL50、CD4和CD8表达明显高于对照组,且有显著性差异(P<0.01),但CD40L表达无显著性差异(P>0.05)。结论:CD40/CD40L、B7/CD28、GL50等共刺激分子表达异常以及局部CD4+和CD8+/T淋巴细胞浸润异常可能与HT甲状腺滤泡细胞破坏和功能减退有关。     

桥本氏甲状腺炎与Graves病的对比观察

作者对50例桥本氏甲状腺炎(HT)和50例Graves病(GD)作了临床及形态学方面的对比观察。按Sato氏分类标准把HT分为单纯型HT和HT伴甲亢;依淋巴细胞浸润等的不同,将单纯型HT、HT伴甲亢和有明显淋巴细胞浸润的GD分为PO、+、++、+++、++++。结果表明GD年龄最轻,单纯型HT最大,HT伴甲亢介于两者之间。从GD到单纯型HT淋巴细胞浸润、滤泡萎缩和纤维组织增生程度逐渐加重,间质血管量减少。提示GD、HT伴甲亢和单纯型HT可能为同一病因作用下而出现的不同临床病理过程,GD为疾病早期,单纯型HT为晚期,HT伴甲亢则为由GD向单纯型HT发展的过渡状态。     

桥本甲状腺炎甲状腺组织TRAIL、Caspase-3的表达

目的 研究桥本甲状腺炎(HT)患者甲状腺组织中肿瘤坏死因子相关凋亡诱导配体(TRAIL)、天冬氨酸特异性半胱氨酸蛋白酶-3(caspase-3)的表达及其在HT发病和病理改变中的意义. 方法 采用S-P免疫组织化学方法检测26例HT(HT组)和12例正常甲状腺组织(对照组)中TRAIL、caspase-3的表达情况. 结果 (1)TRAIL、caspase-3在HT组呈高表达,多见于浸润淋巴细胞旁的甲状腺滤泡上皮细胞;而浸润的淋巴细胞TRAIL染色阴性,caspase-3染色呈弱阳性.(2)TRAIL的表达阳性率在HT组明显高于对照组(72.92%vs 41.67%,P＜0.05),前者滤泡上皮细胞的表达强度明显高于后者[(0.051±0.016)vs (0.016±0.010),P＜0.05].(3)caspase-3的表达阳性率在HT组明显高于对照组(92.31%vs 33.33%,P＜0.01),滤泡上皮细胞的表达强度明显高于对照组[(0.065±0.025)vs(0.022±0.008),P＜0.05].(4)TRAIL与caspase-3的表达程度呈正相关 (rs=0.631,P=0.001). 结论 TRAIL与caspase-3可能共同参与HT的病理演变过程,通过表达TRAIL激活caspase-3而诱导甲状腺滤泡细胞凋亡,损伤甲状腺组织.     

糖皮质激素对新型冠状病毒肺炎患者T淋巴细胞亚群的影响

目的观察新型冠状病毒肺炎(简称新冠肺炎)患者外周血T淋巴细胞亚群改变的特点及糖皮质激素对其影响。方法对武汉市第一医院收治的进行了T淋巴细胞亚群检测的376例新冠肺炎患者进行回顾性分析,按照临床分型分为普通型、重型、危重型及死亡病例,对重型患者根据是否运用糖皮质激素治疗进行分组对比分析。结果根据病情严重程度,包括普通型患者118例(31.4%),重型患者215例(57.2%),危重型患者43例(11.4%)。死亡6例(1.6%),均为危重型。(1)重型患者与普通型患者比较,总淋巴细胞[(1 359.2±597.9)×10~6比(1 703.7±702.4)×10~6/L,LSD-t=4.786,P0.001]、总T淋巴细胞[(949.2±454.0)×10~6比(1 235.5±555.7)×10~6/L,LSD-t=5.175,P0.001]、CD8~+T细胞[(336.8±189.8)×10~6比(461.7±242.8)×10~6/L,LSD-t=5.332,P0.001]显著减少,CD4~+/CD8~+比值(1.81±0.92比1.64±0.74,LSD-t=1.574,P=0.116)增加无显著差异;危重型患者与重型患者比较,CD4~+/CD8~+比值(2.23±1.24比1.81±0.92,LSD-t=2.627,P=0.009)显著增加,CD8~+T细胞[(232.5±159.8)×10~6比(336.8±189.8)×10~6/L,LSD-t=2.867,P=0.004]显著减少,总淋巴细胞[(1 161.1±583.7)×10~6比(1 359.2±597.9)×10~6/L,LSD-t=1.772,P=0.077]、总T淋巴细胞[(790.5±419.3)×10~6比(949.2±454.0)×10~6/L,LSD-t=1.846,P=0.066]减少,无显著差异;死亡患者与危重型患者比较均无显著差异。(2)在215例重型患者中,与未使用糖皮质激素患者比较,使用糖皮质激素治疗3～5 d后患者总T淋巴细胞[(770.6±480.3)×10~6比(986.3±440.7)×10~6/L,t=2.666,P=0.008]和CD4~+/CD8~+比值(1.30±0.73比1.91±0.92,t=3.771,P0.001)均显著性减少。结论新冠肺炎患者T淋巴细胞亚群变化主要表现为T淋巴细胞数量减少和CD4~+/CD8~+比值增加,且与病情严重程度正相关;糖皮质激素治疗可缓解CD4~+/CD8~+比值上升,但加剧了T淋巴细胞减少。     

桥本甲状腺炎组织中细胞凋亡相关蛋白表达的意义

目的　探讨细胞凋亡相关蛋白在桥本甲状腺炎（HT）发病机制及病理变化中的作用及意义。方法　采用TUNEL法检测HT及非毒性甲状腺肿（NTG）患者各17例甲状腺标本中的细胞凋亡水平,并用免疫组织化学方法检测凋亡相关蛋白Fas,FasL,Bcl-2和Bax的表达及分布。结果　HT组细胞凋亡百分率(32.5%±12.3%)比NTG组(1.3%±0.7%)显著增高（P<0.01）,其甲状腺细胞Fas、FasL、Bcl-2和Bax染色阳性率(88%～94%),也显著高于对照组(35%～47%,P<0.01）。HT中凋亡细胞及Fas、FasL和Bax染色强阳性甲状腺细胞多分布于浸润淋巴滤泡附近,Bcl-2染色强阳性细胞则多分布于远离浸润淋巴滤泡的区域。浸润淋巴细胞中Fas,FasL,Bcl-2和Bax染色均较弱。结论　HT中有较高水平的细胞凋亡,凋亡相关蛋白Fas,FasL,Bcl-2和Bax在甲状腺细胞中呈特征性分布的高表达,而在浸润淋巴细胞中表达较少,这些改变与甲状腺滤泡萎缩、破坏及弥漫性淋巴细胞浸润有关。     

桥本氏甲状腺炎患者滤泡辅助性T细胞的检测及临床意义

目的:检测桥本氏甲状腺炎(HT)患者外周血CD4+ CXCR5+ T细胞的表达情况及临床意义?方法:荧光抗体CD4-FITC?PD-1-PE?CXCR5-AF标记外周血细胞,流式细胞术测定49例HT患者?22例正常对照人群CD4+ T细胞表面CDXCR5?PD-1的表达情况?结果:①与正常对照组比较,HT患者CD4+ CXCR5+/CD4+ T显著升高,两者比较有统计学差异(t = 11.158,P < 0.001);CD4+CXCR5+ PD-1+/CD4+ T亦显著高于正常对照,两者比较亦有统计学差异(t = 4.657,P < 0.001);②HT患者CD4+ CXCR5+/CD4+ T细胞与A-TG?A-TPO均呈正相关(r = 0.288,P = 0.045;r = 0.396,P = 0.005),CD4+CXCR5+PD-1+/CD4+ T细胞与A-TG?A-TPO均呈正相关(r = 0.415,P = 0.003;r = 0.355,P = 0.013)?结论:外周血滤泡辅助性T细胞频率升高可能在桥本氏甲状腺炎发病机制中起重要作用?     

肿瘤浸润T淋巴细胞在乳腺癌原发灶中的表达与预后的关系

目的研究肿瘤浸润T淋巴细胞在乳腺癌原发灶中的表达及其与预后的关系。方法回顾性收集乳腺癌患者105例临床资料、病理资料和石蜡包埋病理标本,采用免疫组化检测CD3+T淋巴细胞、CD4+T淋巴细胞、CD8+T淋巴细胞在乳腺癌原发灶的表达,采用COX单因素和多因素分析无病生存率(DFS)和总生存率(OS)相关因素。结果 105例患者乳腺癌原发灶CD3+阳性101例(96.19%),CD4+阳性55例(52.38%),CD8+阳性71例(67.62%),CD3+T淋巴细胞浸润与年龄、肿瘤直径、临床分期、SBR分级、ER表达、PR表达、HER-2表达、淋巴结状态无关,CD4+T淋巴细胞浸润与SBR分级、HER-2表达有关(P<0.05),CD8+T淋巴细胞浸润与SBR分级有关(P<0.05)。单因素分析显示,临床分期、SBR分级、HER-2阳性、淋巴结转移、CD4+T淋巴细胞浸润、CD8+T淋巴细胞浸润与DFS有关(P<0.05);临床分期、SBR分级、HER-2阳性、淋巴结转移、CD4+浸润、CD8+浸润与OS有关(P<0.05);多因素分析显示,CD4+T淋巴细胞浸润、CD8+T淋巴细胞浸润是DFS的保护因素(HR=0.655、0.534,P<0.05);CD4+T淋巴细胞浸润、CD8+T淋巴细胞浸润是OS的保护因素(HR=0.525、0.628,P<0.05)。结论乳腺癌原发灶普遍存在CD3+T淋巴细胞浸润,CD4+T淋巴细胞、CD8+T淋巴细胞浸润与病变程度有关,两者均与乳腺癌较好预后有关。     

移植肝组织淋巴细胞表型分析对急性排斥反应诊断的价值

目的 检测移植肝组织浸润淋巴细胞的免疫表型,分析不同表型淋巴细胞数量及其分布与并发症的关系.方法 应用CD8、CD4、CD3、CD20、CD45RO及CD45RA单抗对108例次移植肝活检组织进行免疫组化染色,对比形态学观察,分析不同区域浸润淋巴细胞的免疫表型.结果 排斥组62例次,非排斥组46例次.排斥组汇管区CD3 、CD8 、CD20 细胞浸润程度均显著高于非排斥组(P＜0.01),两组间各型淋巴细胞在小叶内浸润程度均无显著差异(P＞0.05).排斥反应组中,CD8 细胞浸润程度显著高于CD4 细胞(P＜0.05).排斥组CD3 、CD8 、CD45RO 细胞胆管或血管浸润率显著高于非排斥组(P＜0.01).排斥组中,汇管区CD8 和CD45RO 细胞浸润程度与排斥反应组织学分级显著相关(r值分别为7.481,9.103,P＜0.01).结论 移植肝活检组织中淋巴细胞免疫学分型对排斥反应的诊断和鉴别诊断具有一定的指导意义.     

COPD患者T淋巴细胞亚群比例及其与BODE指数和急性加重风险的相关性

目的:探讨慢性阻塞性肺疾病(COPD)患者外周血T淋巴细胞亚群的比例,判定其与BODE指数及急性加重风险的相关性。方法:分别选择69例COPD患者(吸烟者44例,非吸烟者25例)和50例健康志愿者,采用流式细胞仪检测两组受试者外周血T淋巴细胞亚群;分析COPD患者的BODE指数及1年随访期内COPD患者急性加重住院治疗次数与T淋巴细胞亚群的相关关系。结果:COPD组外周血CD3~+、CD4~+T淋巴细胞和CD4~+/CD8~+比例均低于健康志愿组(P<0.01),而CD8~+T淋巴细胞无明显改变(P>0.05);COPD吸烟者外周血CD4~+T淋巴细胞和CD4~+/CD8~+比例明显低于COPD非吸烟者(P<0.01),CD3~+、CD8~+T淋巴细胞与COPD非吸烟者相比无差异性(P>0.05)。CD4~+T淋巴细胞和CD4~+/CD8~+比例与BODE指数显著负相关(r=-0.440、P=0.000;r=-0.456、P=0.000),而CD3~+、CD8~+T淋巴细胞与BODE指数无明显相关性(r=-0.200、P=0.099;r=-0.207、P=0.088);CD3~+、CD4~+T淋巴细胞和CD4~+/CD8~+水平与COPD急性加重次数呈明显负相关(r=-0.264、P=0.028;r=-0.296、P=0.013;r=-0.245、P=0.042),而CD8~+T淋巴细胞与COPD急性加重次数无明显相关性(r=-0.005、P=0.967)。结论:CD4~+T淋巴细胞和CD4~+/CD8~+水平可能与COPD的严重程度和COPD急性加重密切相关,且吸烟影响COPD患者外周T淋巴细胞亚群的比例。     

The attenuative effect of purified protein derivative sensitization on T helper 2 reaction and eosinophil infiltration of the lung in ovalbumin sensitized mice

OBJECTIVE To identify the effects of tuberculin purified protein derivative (PPD) sensitization on attenuating pulmonary T helper 2 (Th2) reaction and eosinophil infiltration in ovalbumin sensitized mice, and to search for the possibility of its clinical use in the management of asthma in a new way.

METHODS Sixty C57BL/6 mice were sensitized with PPD and then with ovalbumin and aluminum hydroxide, and randomized into 4 groups: ovalbumin (OVA), pre-PPD, post-PPD and control groups. Aerosol PPD were administered 3 h before or after ovalbumin challenge in the pre-PPD and post-PPD groups respectively, and control group received aerosol PPD only. IL-4, IL-5 expression was detected by immunocytochemistry in situ hybridization. Lung slides were stained with eosin and hemotoxylin, and pathological changes were observed.

RESULTS Ovalbumin aerosol inhalation caused a mixed inflammatory infiltration dominated by CD4+ T lymphocytes and eosinophils in the lung of sensitized mice. 87.5%-89.7% and 89.0%-89.2% of the CD4+ T lymphocytes were IL-4 mRNA+ and IL-5 mRNA+ respectively. 88.7%-91.2% of IL-4 mRNA+ cells and 89.8%-90.6% of IL-5 mRNA+ cells were CD4+ T lymphocytes in OVA group. Aerosol administration of PPD markedly suppressed IL-4 and IL-5 expression, and lung eosinophil infiltration. It was more effective in pre-PPD group. 76.6%-78.0% of IL-4 mRNA+ and 73.8%-79.7% of IL-5 mRNA+ cells were CD4+ and 78.1%-84.9% and 78.4%-85.3% of the CD4+ cells were IL-4 mRNA+ or IL-5 mRNA+ respectively in pre-PPD group, both were markedly lower than that of OVA group. CD4+ percentage of IL-4 mRNA+ and IL-5 mRNA+ cells were 80.7%-82.0% and 78.0%-83.9% in post-PPD group, which were markedly lower than that of OVA group.

CONCLUSIONS Sensitization with PPD by intraperitoneal injection and then challenged by PPD inhalation markedly suppressed IL-4, IL-5 expression and eosinophil infiltration, and attenuated pulmonary Th2 reaction in ovalbumin sensitized mice. This induces Th1 type reaction and inhibits Th2 cell differentiation. It may be beneficial for glucocorticoids dependent or resistant patients.

     

CD8+CD28-T细胞在哮喘小鼠发病机制中的作用及地塞米松对其的影响

目的 探讨CD8+CD28-T细胞在哮喘发病机制中的作用及地塞米松对该细胞的影响.方法 30只BALB/c小鼠随机分为哮喘组、地塞米松组、正常对照组,各10只.哮喘组和地塞米松组给予卵白蛋白致敏后雾化吸入卵白蛋白溶液,地塞米松组每次雾化吸入前腹腔注射地塞米松1 mg/kg,各组分别于末次雾化激发后测定小鼠的气道反应性;对支气管肺泡灌洗液(BALF)行细胞总数、嗜酸性粒细胞(EOS)计数;取肺组织作HE染色病理切片;测BALF中IgE含量;流式细胞仪检测小鼠血、BALF中CD8+CD28-T细胞占淋巴细胞百分比;分析BALF中IgE、EOS计数与血液中CD8+CD28-T细胞百分比的相关性.结果 哮喘组、地塞米松组气道反应性明显高于正常对照组.哮喘组BALF中细胞总数和EOS计数分别为(5.56±4.06)× 102/L和(3.29±2.23)× 102/L,均明显高于地塞米松组[(2.59±1.69)× 102/L,P=0.044和(1.11±0.73)×102/L,P=0.008]及正常对照组[(0.91±0.65)×102/L,P=0.003和(0.43±0.37)× 102/L,P=0.001)];而后两组之间差异均无统计学意义(均P>0.05).哮喘组、地塞米松组、正常对照组BALF中IgE含量分别为(23.85±5.97)g/L、(13.15±2.22)g/L、(6.54±1.03)g/L,三组间差异有统计学意义(F=38.558,P=0.000).哮喘组、地塞米松组、正常对照组CD8+CD28-T细胞百分比在外周血中分别为(18.68±4.12)%、(13.43±2.90)%、(8.43±4.60)%;在BALF中分别为(1.25±0.40)%、(0.66±0.49)%、(0.21±0.19)%,组间差异均有统计学意义(F=11.837,P=0.001;F=12.885,P=0.000).哮喘组BALF中IgE含量和EOS计数与外周血中CD8+CLY28-T细胞百分比均呈正相关(r=0.864,P=0.012和r=0.804,P=0.029).结论 CD8+CD28-T细胞数量与哮喘小鼠气道炎症有明显相关性,地塞米松可有效抑制哮喘气道炎症并可能抑制了CD8+CD28-T细胞的表达和功能.

Abstract：

Objective To explore whether or not CD8+ CD28- T cell play a pathogenic role in asthma and detect the effects of dexamethasone ( DXM ). Methods A total of 30 mice were randomly divided into 3 groups: asthmatic group, DXM group and control group ( n = 10 each). The asthmatic and DXM groups were sensitized twice and inhaled ovalbumin. The DXM Group received an intraperitoneal injection of DXM lmg/kg before inhaling ovalbumin. After successful modeling, 3 mice were selected randomly from each group to measure the airway responsiveness. Also a bronchoalveolar lavage cytological study was performed and lung tissue sections were prepared for histopathologic examination to evaluate the airway inflammation. The content of IgE in bronchoaleolar lavage fluid ( BALF) was detected with a murine IgE ELISA kit. And the fractions of CD8 + CD28- T cell of peripheral blood and BALF were tested by flow cytometry to analyze the correlation between IgE, eosinophils ( EOS) of BALF and CD8 + CD28 - T cell of blood. Results The airway hyperresponsiveness in asthmatic and DXM groups were significantly higher than that in the control group. The number of total cells and EOS of BALF in the asthmatic group [ ( 5. 56 ±4. 06) × 102/L; (3. 29 ±2. 23) × 102/L] were significantly higher than that in control group [ (0. 91 ±0.65)×102/L, P = 0.003; (0.43 ±0.37) × 102/L, P = 0.001] and DXM group [(2.59 ±1.69) ×102/L, P =0.044; (1. 11 ±0.73) ×l02/L, P = 0.008]; while the DXM group was insignificantly higher than the control group (P=0. 234, P=0. 363). There were significant differences in the contents of IgE of BALF for the asthmatic, DXM and control groups [ (23. 85 ±5. 97) g/L, (13. 15 ±2.22) g/L, (6.54±1. 03) g/L, F = 38. 558, P = 0. 000 ] . The percentages of CD8 + CD28- T cell in peripheral blood in asthmatic and DXM groups [ (18. 68 ±4. 12)% and ( 13.43 ± 2. 91) % ] were significantly higher than those in control mice [ (8. 43 ± 4. 60) % , both P < 0. 05 ]. The percentages of CD8 + CD28 - T cell of BALF in asthmatic group and DXM group [(1.25±0. 40)% and (0. 66 ± 0. 49) % ] were also significantly higher than those in control mice [ (0. 21 ± 0. 19) % , both P < 0. 05 ]. The percentages of CD8 + CD28 - T cell of blood and BALF in the DXM mice were significantly lower than those in asthmatic group. The correlations between IgE ( r = 0. 864, P = 0. 012), EOS ( r = 0. 804, P = 0.029) and CD8 + CD28- T cell were significant. Conclusion The fraction of CD8 + CD28- T cell is closely correlated with the inflammation of asthmatic airway. The airway hyperresponsiveness and inflammation in asthmatic mice may be relieved by DXM through its effect of inhibiting the expression of CD8 + CD28- T cell.     

类风湿关节炎患者CD8+IL-17+T细胞升高及其机制

目的 探讨CD8+IL-17+T细胞在类风湿关节炎(RA)的改变及可能的机制.方法 随机采集39例RA患者和40名健康人的外周血.以流式细胞术测定全部RA患者和27名健康人的外周血CD8+IL-17+T细胞的比例;以ELISA方法测定全部RA患者和健康人的血清白细胞介素(IL)6、IL-23和IL-17水平,并分析这些指标可能的相瓦关系.结果 RA患者CD8+IL-17+T细胞在CD8+T细胞的比例中位数为2.7%,95%可信区间为1.55%-3.74%;而正常人中位数为1.61%,95%可信区间为1.25%-2.61%.RA患者外周血CD8+IL-17+T细胞升高(P<0.05).对CD8+IL-17+T细胞功能相关的IL-17水平测定结果为,RA患者为(429±502)ng/L,而正常人仅为(13±30)ns/L(P<0.01).RA患者血清IL-17水平明显升高.对于CD8+IL-17+T细胞分化相关细胞因子的血清测定结果,IL-23水平在RA患者为(157.83±27.07)ns/L,正常人为(21.97±3.52)ns/L(P<0.01);IL-6水平在RA患者为(32.67±34.50)ns/L,正常人为(1.82±1.51)ns/L(P<0.01);RA患者血清IL-6、IL-23水平明显升高.结论 RA患者CD8+IL-17+T细胞数量增多,作用增强,IL-6和IL-23的升高是引起这些改变的可能原因.     

重症肌无力患者外周血CD4+ CD25+调节性T细胞与抗乙酰胆碱受体抗体和转化生长因子β1含量的相关性

目的 探讨重症肌无力(MG)患者外周血CD4+CD25+调节性T(Treg)细胞数量与血清抗乙酰胆碱受体抗体(AChR-Ab)和转化生长因子(TGF)-β1含量的相关性.方法 前瞻性地纳入40例新近发病或加重的MG住院患者和38名年龄、性别匹配的健康对照,应用流式细胞仪检测外周血CD4+ CD25+ Treg细胞数量,酶联免疫法检测血清TGF-β1含量,放免法检测血清AChR-Ab滴度,并对三者进行了相关性分析.结果 MG患者外周血CD4+CD25+Treg细胞百分率(3.0%±2.5%)显著低于健康对照(4.6%±3.7%,P=0.03).发病晚、病程长、抗AChR-Ab阳性、胸腺正常或退化以及未接受胸腺切除治疗等因素与MG患者CD4+CD25+Treg细胞减低有关.在31例非胸腺瘤MG(non-MGT)患者中,血清TGF-β1含量(112 ng/L±83 ng/L)显著低于健康对照(215 ng/L±134 ng/L,P=0.00),但在MG各临床亚型之间差异无统计学意义.虽然MG患者CD4+ CD25+Treg细胞百分率与血清AChR-Ab滴度不呈线性相关,但在非MGT患者中二者呈负相关(r=-0.37,P=0.02).非MGT患者血清AChR-Ab滴度还与Osserman临床分型和MGFA评分之间呈正相关(均r=0.34,P=0.03).非MGT患者血清TGF-β1含量与美国MG协会(MGFA)评分和CD4+CD25+Treg细胞百分率无相关性.结论 MG患者外周血CD4+CD25+Treg细胞百分率和血清TGF-β1含量均明显低于健康对照,可能参与了MG的发病.非MGT患者中Treg细胞百分率与AChR-Ab滴度呈负相关,检测其水平可能对评估MG病情及治疗提供理论依据,但是应用于临床还需要更多的相关研究.     

Aerosol administration of dexamethasone and methotrexate attenuated Th2 reaction and eosinophil infiltration of the lung in ovalbumin sensitized mice

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生脉注射液对创伤失血性休克大鼠免疫功能的影响

目的探讨生脉注射液对创伤失血性休克大鼠T淋巴细胞及其亚群的影响,为揭示生脉注射液调理创伤后免疫功能紊乱机制提供依据。方法制作创伤失血性休克大鼠模型。将30只SD大鼠随机分为3组,分别为正常对照组（A组）、创伤失血性休克组（B组）、生脉注射液治疗组（C组）,每组各10只。3组大鼠分别于实验开始后第3天处死。全自动血液生化仪检测大鼠血常规,流式细胞仪检测T淋巴细胞及其亚群（CD3^＋、CD4^＋、CD8^＋）含量。结果大鼠创伤失血性休克后,机体出现过度的炎症反应和免疫功能低下状态,B组与A组比较,白细胞含量显著升高[（8.890±0.387）×10^9/L vs（4.230±0.856）×10^9/L,P=0],中性粒细胞比例显著升高[（26.15±2.97）%vs（16.00±4.53）%,P=0],淋巴细胞比例显著下降[（68.57±5.23）%vs（76.617±4.9）%,P=0.001]。应用生脉注射液治疗后,C组与B组比较,白细胞明显下降[（6.29±0.758）×10^9/L vs（8.89±0.387）×109/L,P=0],中性粒细胞比例显著下降[（20.29±3.09）%vs（26.15±2.97）%,P=0.001],同时,淋巴细胞比例显著上升[（74.85±4.12）%vs（68.57±5.23）%,P=0.007]。创伤失血性休克后,B组与A组相比,大鼠CD3^＋、CD4^＋T淋巴细胞数量显著降低[CD3＋：（31.17±4.00）vs（41.97±2.50）,P=0;CD4^＋：（10.49±1.42）vs（15.51±3.48）,P=0.003],CD4^＋/CD8^＋比值降低[（0.97±0.09）vs（1.19±0.07）,P=0],CD8＋含量变化差异无统计学意义[（17.75±5.94）vs（17.34±3.77）,P=0.997]。大鼠处于免疫功能抑制状态,在生脉注射液治疗后,C组与B组比较,CD3^＋、CD4^＋T细胞数量显著升高[CD3^＋：（36.64±5.73）vs（31.17±4.00）,P=0.001;CD4^＋：（10.49±1.42）vs（13.94±2.02）,P=0.008],CD4^＋/CD8^＋比值有所升高[（1.12±0.03）vs（0.97±0.09）,P=0.001]。结论创伤失血性休克大鼠出现炎症反应和T淋巴细胞免疫功能下降,应用生脉注射液能明显提高创伤失血性休克大鼠T淋巴细胞的免疫功能,降低炎症反应。     

慢性胃炎CD4+T、CD8+T细胞及Foxp3的表达及意义

目的:通过检测人慢性胃炎中CD4+T、CD8+T细胞及Foxp3的表达情况,探讨免疫细胞及分子在疾病进展过程中变化情况及对疾病发展的影响。方法:收集胃镜下钳取20例浅表性胃炎（其中Hp阳性10例,Hp阴性10例）,20例萎缩性胃炎（其中Hp阳性10例,Hp阴性10例）标本。采用免疫组织化学方法检测CD4+T、CD8+T细胞及Foxp3的表达。结果:Hp阳性萎缩性胃炎胃黏膜中CD4+T细胞、CD8+T细胞、Foxp3的表达均高于Hp阴性萎缩性胃炎及Hp阳性浅表性胃炎胃黏膜中的表达（P<0.01）。Hp阳性胃炎（浅表+萎缩）胃黏膜中CD4+T细胞、CD8+T细胞、Foxp3的表达量均高于Hp阴性胃炎（浅表+萎缩）胃黏膜中的表达（P<0.01）。Hp阳性浅表性胃炎胃黏膜中CD4+T细胞的表达高于Hp阴性浅表性胃炎胃黏膜中的表达（P<0.01）,Hp阳性浅表性胃炎胃黏膜组中CD8+T细胞和Foxp3的表达与Hp阴性浅表性胃炎胃黏膜中的表达差异均无统计学意义（P>0.05）。结论:Hp感染阳性胃炎胃黏膜中T淋巴细胞亚群CD4+T细胞、CD8+T细胞的浸润和Foxp3表达均高于Hp阴性胃炎,且Hp感染阳性胃炎胃黏膜中,萎缩性胃炎T淋巴细胞亚群及Foxp3表达均高于浅表性胃炎。     

冷冻消融联合栓塞治疗对中晚期肾癌细胞免疫功能的影响

目的 分析氩氦冷冻消融联合肾动脉栓塞(TRAE)治疗对中晚期肾癌患者外周血CD4~+CD25~+调节性T细胞(regulatory T cell,Treg)的影响及临床意义.方法 回顾我院77例中晚期肾癌患者临床资料,依据接受治疗方式分为两组:冷冻消融联合TRAE治疗组32例;单纯TRAE组45例.分别于治疗前、后3个月取外周血,流式细胞仪检测外周血Treg及T淋巴细胞亚群;术后1个月采用增强MRI或CT评价肿瘤坏死程度.结果 联合组治疗后Treg细胞占CD4~+T细胞比例由6.6%±1.2%下降至3.9%±1.2%,二者差异具有统计学意义(t=42.768,P<0.01);CD4~+T、CD8~+T细胞比例及CD4~+T/CD8~+T较术前明显增高,差异均具有统计学意义(均P<0.01).而TRAE组治疗前后Treg细胞占CD4~+T细胞比例、CD4~+T、CD4~+T/CD8~+T、CD8~+T细胞比例虽略有增高但差异均无统计学意义(均P>0.05).联合组的肿瘤坏死率为57.5%,单纯TRAE组为31.6%,两组比较,差异具有统计学意义(t=6.784,P<0.01).联合组中位生存期为(20个月),明显高于TRAE组(12个月),二者差异具有统计学意义(χ~2=7.368,P<0.01).相关性分析显示:治疗后Treg细胞比例下降程度与肿瘤坏死率(r=0.90 P<0.01)及生存期(r=0.67 P<0.01)呈密切正相关关系.结论 TRAE与冷冻消融联合治疗中晚期肾癌能明显降低Trcg细胞比例,改善患者免疫状态,可提高肿瘤坏死率并延长患者生存期.     

Identification of correlations between numbers of CD4+ CD25+ Treg cells, levels of sera anti-AChR antibodies and transfer growth factor-beta in patients with myasthenia gravis

OBJECTIVE: The purpose of the current study is to demonstrate possible involvement of CD4+ CD25+ Treg cells and TGF-beta in immune activation in patients with myasthenia gravis (MG). If so, how does CD4+ CD25+ Treg cells and TGF-beta, collaborate to impact on the production of pathogenic anti-AChR antibodies (Ab)? METHODS: 40 MG in-patients with recent onset or deterioration and age and gender-matched 38 healthy subjects were consecutively enrolled. Flow cytometry was employed to detect circulating CD4+ CD25+ Treg cells. Levels of AChR-Abs and TGF-beta1 in serum were detected by radioimmunoassay and enzyme-linked immunoabsorbance assay respectively. RESULTS: Numbers of CD4+ CD25+ Treg cells were significantly decreased in MG patients (3.0% +/- 2.5%) compared with healthy controls(4.6% +/- 3.7% , P = 0.03). Decreased production of CD4+ CD25+ Treg cells was associated with late-onset, longer-duration, positive-MG sera for AChR-Abs, normal or atrophic thymus, and non-thymectomy treatment et al, respectively. Although CD4+ CD25+ Treg cells were not linear-correlated with serum anti-AChR Ab titers, but were conversely correlated with each other in MG patients without thymoma (non-MGT) (r = -0.37, P = 0.02). Likewise, levels of TGF-beta1 in 31 non-MGT patients (112 ng/L +/- 83 ng/L) were decreased compared with those of healthy subjects (215 ng/L +/- 134 ng/L, P = 0.00), and was conversely correlated with titers of anti-AChR Abs (r = -0.37, P = 0.02). The titer of anti-AChR Abs were correlated with Osserman classification and MGFA grade (r = 0.34, P = 0.03). CONCLUSION: Numbers of CD4+ CD25+ Treg cells and levels of TGF-beta1 in MG patients were significantly decreased compared with healthy controls, and may thus contribute to the pathogenesis of MG. Numbers of CD4+ CD25+ Treg cells were conversely correlated with levels of anti-AChR Abs in non-MGT patients.