再生障碍性贫血和骨髓增生异常综合征患者骨髓CD34+细胞及其粒细胞集落刺激因子受体的研究

目的:检测再生障碍性贫血(AA)和骨髓增生异常综合征(MDS)患者CD34 细胞占骨髓单个核细胞(BMMNC)的比率及其表面粒细胞集落刺激因子受体(G-CSFR)的表达率。方法:用流式细胞术(FCM)检测13例AA、22例MDS及12例非血液病患者CD34 细胞占BMMNC的比率及其表面G-CSFR的表达率。结果:AA组与对照组、AA组与MDS组、MDS-难治性贫血(RA)组与难治性贫血伴原始细胞增多(RAEB)组BMMNC中CD34 细胞的比率比较差异有统计学意义(P<0.05),但G-CSFR的表达率差异无统计学意义(P>0.05)。多数重型AA(SAA)患者(3/4)及少数慢性AA(CAA)患者(1/9)BMMNC中的CD34 细胞少于0.1%。多数G-CSFR表达率低(<14%)的患者(7/9)外周血中性粒细胞减少;而表达率正常(14.0%~28.9%)的患者(1/6)很少见;表达率高(>28.9%)的患者(3/7)也可存在中性粒细胞减少。结论:造血干细胞减少是AA的主要发病机制之一,其表面G-CSFR的表达率不是影响AA的主要因素;MDS患者CD34 细胞比率升高是一个预后不良的指标,G-CSFR的检测可部分解释MDS患者外周血中性粒细胞减少的原因。     

AA和MDS患者骨髓CD+34细胞及G-CSFR的表达及意义

目的检测再生障碍性贫血(AA)和骨髓增生异常综合征(MDS)患者骨髓CD+34细胞占单个核细胞(MNC)的比率及其表面粒细胞集落刺激因子受体(G-CSFR)的表达率,以探讨二者可能的发病机制.方法用流式细胞术(FCM)检测13例AA、22例MDS及12例非血液病患者骨髓CD+34细胞占MNC的比率及其表面G-CSFR的表达率.结果 AA组与对照组、AA组与MDS组、MDS-难治性贫血(RA)组与MDS-难治性贫血伴原始细胞增多(RAEB)组的骨髓MNC中CD+34细胞比率比较有显著性差异(P＜0.05),但G-CSFR的表达率比较无显著性差异(P＞0.05).大多数重型AA(SAA)患者(3/4)及很少慢性AA(CAA)患者(1/9)的骨髓MNC中CD+34细胞比率小于0.1%.大多数G-CSFR表达率低(＜14%)的MDS患者(7/9)外周血中性粒细胞减少;中性粒细胞减少在G-CSFR表达率正常(14%～28.9%)的患者(1/6)很少见;G-CSFR表达率高(＞28.9%)的患者(3/7)也存在中性粒细胞减少.结论骨髓CD+34细胞检测有助于判断AA患者病情及MDS患者的预后,亦可用于鉴别AA和MDS.     

AA和MDS患者骨髓CD+34细胞表面GM-CSFR的表达及意义

目的 探讨再生障碍性贫血（AA）和骨髓增生异常综合征（MDS）患者骨髓CD34^＋细胞表面粒细胞-巨噬细胞集落刺激因子受体（GM—CSFR）的表达情况。方法 用流式细胞术（FCM）和单克隆抗体技术检测14例AA、23例MDS和8例非血液病患者骨髓CD34^＋细胞表面的GM—CSFR表达率。结果 MDS组骨髓CD34^＋细胞表面GM-CSFR的表达率明显高于对照组及AA组（P〈O．05）,而AA组与对照组间差异无统计学意义（P〉0．05）。结论 AA患者造血干细胞没有质的缺陷;造血干细胞异常可能是MDS的主要发病机制之一。     

急性白血病细胞G-CSF、GM-CSF受体的检测及其临床意义

目的：研究急性白血病（AL）患者骨髓单个核细胞表面粒细胞集落刺激因子受体（G-CSFR）与粒-巨噬细胞集落刺激因子受体（GMCSFR）的表达规律。观察重组人粒细胞集落刺激因子（rhG-CSF）在AL中应用的临床疗效。方法：采用流式细胞术检测15例正常对照和86例AL患者G-CSFR、GM—CSFR的表达率。观察rhG-CSF的应用对AL治疗的影响。结果：急性非淋巴细胞白血病（ANLL）患者G-CSFR、GM—CSFR的表达率明显高于急性淋巴细胞白血病（ALL）（P〈0．01），均低于对照组。AL患者G-CSFR与GMCSFR表达率无相关性（rs=0．127，P〉0．20）；ANLL患者，G-CSFR表达率与CD13、MPO表达率呈正相关（P〈0．01），与CD33表达率呈负相关（P〈0．01），GM-CSFR表达率与HLA-DR表达率呈正相关（P〈0．01）。ALL患者。GM—CSFR的表达率与CD19的表达率呈正相关（P〈0．01）。应用rhG-CSF能减少AL患者中性粒细胞缺乏及发热的天数，但对缓解率无影响。结论：G-CSFR、GM—CSFR．的表达率在ANLL与ALL中有差异，两者的表达无相关性，在化疗过程中及化疗后应用rhG-CSF对AL的缓解率无显著影响。     

Neutrophil function and cytokine-specific signaling in chronic neutrophilic leukemia

We diagnosed an 86-year-old woman with chronic neutrophilic leukemia (CNL) because she showed sustained leukocytosis dominated by mature neutrophils, hepatosplenomegaly, high neutrophilic alkaline phosphatase score, absence of the Ph chromosome, low serum level of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF), and no evidence of leukemoid reaction. We found that the extent of stimulation of her neutrophil functions by G-CSF and GM-CSF was greatly reduced compared to healthy donars neutrophils. We showed that CNL neutrophils have intact expression of granulocyte colony-stimulating factor receptor (G-CSFR) and granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR). This suggests that failure of enhancement by G-CSF and GM-CSF in CNL neutrophil functions might be due to disturbances in the intracellular domains of G-CSFR and GM-CSFR, regardless of external cytokine stimulation. However, the patient's neutrophils did not show any mutations in the G-CSFR and GM-CSFR intracellular critical regions. We also showed that stat3 and mitogen-activated protein kinase activation by G-CSF or GM-CSF in the patient's neutrophils were significantly lower than those in healthy donor neutrophils. These results suggest that deficiency of CNL neutrophil function might be due to insufficiency of some inflammatory cytokine-specific signaling. Hence, we are the first to show that CNL neutrophils have partially insufficiency in some cytokine-specific signaling. Further studies are needed to elucidate the signal transduction pathways relating to functional defects in CNL neutrophils.     

Exclusive expression of G-CSF receptor on myeloid progenitors in bone marrow CD34+ cells

Although granulocyte colony-stimulating factor (G-CSF) has been reported to act on cells of neutrophilic lineage, the administration of G-CSF to induce the mobilization of various haematopoietic progenitors into the circulation. We analysed the expression of receptors for G-CSF (G-CSFR) on human bone marrow and G-CSF-mobilized peripheral blood CD34+ cells, and examined the proliferation and differentiation capabilities of sorted CD34+G-CSFR+ and CD34+G-CSFR- cells using methylcellulose clonal culture. Flow cytometric analysis showed that G-CSFR was expressed on 14.9 +/- 4.9% of bone marrow CD34+ cells, most of which were included in CD34+CD33+ and CD34+CD38+ cell fractions. In clonal cultures, CD34+G-CSFR+ cells produced only myeloid colonies, whereas CD34+G-CSFR- cells produced erythroid bursts, megakaryocyte and multilineage colonies. When incubated with the cytokine cocktail for 5 d, CD34+G-CSFR- cells generated CD34+G-CSFR+ myeloid progenitors. In G-CSF-mobilized peripheral blood, CD34+ cells contained 10.8 +/- 5.8% of G-CSFR+ cells, most of which were also myeloid progenitors, although CD34+G-CSFR- cells contained a substantial number of myeloid progenitors. These results indicated that the expression of G-CSFR on CD34+ cells is restricted to myeloid progenitors, suggesting that the specific activity of G-CSF on myelopoiesis depends on the exclusive expression of its receptor on myeloid progenitors, and that the mobilization of various haematopoietic progenitors is not a direct effect of G-CSF in humans.     

骨髓增生异常综合征T细胞早期激活及可溶性肿瘤坏死因子受体的研究

目的　研究骨髓增生异常综合征 (MDS)外周血CD+ 4 、CD+ 8T细胞早期激活标志CD69的表达及血清、骨髓可溶性肿瘤坏死因子受体 1、2 (sTNF R1、2 )的水平及其意义。方法　在植物血凝素 (PHA) 2 0mg/L条件下进行全血细胞培养 ,于 0h和 4h分别用流式细胞仪对CD+ 4 、CD+ 8T细胞CD69的表达进行分析。用ELISA法检测血清和骨髓sTNF R1、2的水平。结果　PHA刺激前难治性贫血 (RA)与难治性贫血伴环形铁粒幼细胞增多 (RAS)CD+ 4 、CD+ 8细胞CD69的表达率分别为 8 32 %、9 88% ,难治性贫血伴原始细胞增多 (RAEB)与转变中的RAEB(RAEB T)CD+ 8细胞CD69的表达率为7 92 %。PHA刺激后MDS患者CD+ 4 、CD+ 8细胞表达CD69明显增强 ,RA +RAS为 5 3 4 6 %、5 1 6 3% ;RAEB +RAEB T为 4 2 93%、4 1 96 % ,CD+ 4 与CD+ 8细胞CD69的表达率相似。MDS两种sTNF R1水平均明显升高 ,RA +RAS组sTNF R1血清为 (1 5 8± 0 6 8) μg/L ,骨髓为 (2 10± 0 2 6 ) μg/L ;sTNF R2血清为 (1 4 1± 0 5 0 ) μg/L ,骨髓为 (1 95± 0 6 4 ) μg/L ;RAEB +RAEB T组sTNF R1血清为 (2 6 2± 2 5 5 ) μg/L ,骨髓为 (3 12± 0 6 7) μg/L ;sTNF R2血清为 (1 96± 0 5 6 ) μg/L ,骨髓为(3 0 9± 0 6 2 ) μg/L。血清sTNF R2水平与PHA刺激     

Flow cytometric evaluation of circulating CD34+ cell counts and apoptotic rate in children with acquired aplastic anemia and myelodysplasia

OBJECTIVE: Identification of a rapid and noninvasive test for the follow-up of aplastic anemia (AA) patients during immunosuppressive therapy (IST) to evaluate its functional effect on hematopoietic progenitors (HPC) and for early detection of progression to myelodysplasia or relapse. MATERIALS AND METHODS: Absolute count and apoptotic rate (AR) of peripheral blood (PB) CD34+ cells were evaluated by three-color flow cytometry for CD45, CD34, and annexin V in cord blood (CB), normal children, and adults, as well as in pediatric patients with AA at diagnosis and during IST, Fanconi anemia (FA), chronic immune cytopenia, and refractory anemia with excess blasts (RAEB). RESULTS: In normal subjects, the AR of PB CD34+ cells showed a progressive increase (p < 0.05), while their counts decreased (p < 0.05) from birth to adulthood. In very severe AA (vSAA) and severe AA (SAA) at diagnosis, the AR was 91.6% +/- 2.8%, higher than controls (p < 0.05), and PB CD34+ cell count was 2.6 +/- 2.4/microL. In FA patients, the PB CD34+ AR was again significantly increased (54.2% +/- 13.7%) with an absolute count of 3.7 +/- 1.2/microL. Conversely, in RAEB the AR was 11.7% +/- 3.5% and the absolute count 85.1 +/- 48.2/microL (p < 0.05). Chronic immune cytopenias did not significantly differ from controls. CONCLUSIONS: Flow cytometry evaluation of PB CD34+ AR and counts is a noninvasive and feasible first-step method for the differentiation of AA and myelodysplasia (MDS), and it might be useful for monitoring AA during IST to secure the early detection of relapse or transformation to MDS.     

Immunophenotype of myeloid granulocytes: a pilot study for distinguishing myelodysplastic syndrome and aplastic anemia by flow cytometry

It is often difficult to distinguish myelodysplastic syndrome (MDS) from aplastic anemia (AA) because of the considerable clinical, cytologic histologic similarities between these two disorders; however, distinguishing between AA and MDS is of great importance because there is a higher risk of progression to acute leukemia in patients with MDS compared with AA. Up to now, CD34⁺ cells in MDS and AA patients have been studied extensively; however, little information is available on myeloid granulocytes. The aim of this study was to determine whether immunophenotype of myeloid granulocytes in AA patients was different from that of MDS. Flow cytometry was used to assess the immunophenotype of myeloid granulocytes in 22 patients with MDS, 12 with AA, and 10 normal subjects. Our data showed that the percentages of CD13⁺ granulocytes, CD33⁺ granulocytes, CD34⁺ granulocytes, and HLA-DR⁺ granulocytes were significantly higher in patients with MDS than in AA patients and normal subjects (P < 0.05). The percentages of CD15⁺ granulocytes and CD10⁺ granulocytes were significantly lower in patients with MDS than in AA patients and normal subjects (P < 0.05). There were no significant differences in the expression of these markers between patients with AA and normal subjects (P > 0.05). As refractory anemia progressing to refractory anemia with excess blasts, the percentages of CD13⁺ granulocytes, CD33⁺ granulocytes, CD34⁺ granulocytes and HLA-DR⁺ granulocytes were significantly increased, whereas, the percentage of CD15⁺ granulocytes was significantly decreased (P < 0.05). These data suggest that immunophenotype of myeloid granulocytes may be a useful parameter for the differential diagnosis of MDS and AA.     

骨髓中表达白细胞介素5受体 mRNA的CD+34 细胞与支气管哮喘气道炎症的关系

目的　探讨支气管哮喘 (简称哮喘 )小鼠骨髓 (BM)中表达CD+ 34 与白细胞介素 5受体(IL 5RmRNA+ )的造血细胞 (CD+ 34 IL 5RmRNA+ 细胞 )在气道炎症中的作用。方法　以卵白蛋白(OVA)及生理盐水致敏并激发Balb/c小鼠 ,建立各哮喘及对照组 (A组 )模型。分别于OVA及生理盐水首次激发后 1、6、12、2 4、48h处死小鼠 ,取支气管肺泡灌洗液 (BALF)、外周血 (PB)及BM标本备用。测定BALF中嗜酸性粒细胞 (EOS)、PB中有核细胞及EOS计数及BM中有核细胞数 ;用流式细胞仪分别测定PB及BM中CD+ 34 细胞占相应有核细胞的比例并推算其相对计数 ;用免疫组化结合原位杂交法分别标记骨髓细胞CD+ 34 抗原及IL 5RmRNA ,定位BM中CD+ 34 IL 5RmRNA+ 细胞并计数其占CD+ 34 细胞的比例。结果　 (1)OVA激发后 6h组 ,BALF中EOS计数为 (2 67± 1 0 0 )× 10 5/L ,与A组 [(0 46±0 0 6)× 10 5/L]比较差异有显著性 (P <0 0 1) ;OVA激发后 12h组 ,BALF中EOS、PB中EOS计数分别为 (7 74± 1 98)× 10 5/L、(2 91± 0 64 )× 10 8/L ,与A组 [(0 46± 0 0 6)× 10 5/L、(1 43± 0 3 7)× 10 8/L]比较 ,差异有显著性 (P均 <0 0 1) ;OVA激发后 2 4h组 ,BALF中EOS、PB中EOS计数分别为 (19 43±3 69)× 10 5/L、(3 93± 0 5 1)× 10     

Proteolytic cleavage of granulocyte colony-stimulating factor and its receptor by neutrophil elastase induces growth inhibition and decreased cell surface expression of the granulocyte colony-stimulating factor receptor

Neutrophil elastase (NE) is a serine protease stored in the primary granules of neutrophils that proteolytically cleaves multiple cytokines and cell surface proteins on release from activated neutrophils. Recent reports of mutations in the gene encoding this enzyme in some patients with neutropenic syndromes prompted us to investigate whether granulocyte colony-stimulating factor (G-CSF) and its receptor (G-CSFR) are also substrates for NE. To further address this, we examined the effect of NE on G-CSF and the G-CSFR both in solution and on intact cells. Incubation of recombinant G-CSF or a G-CSFR form corresponding to its extracellular domain with purified NE resulted in rapid proteolytic cleavage of both proteins. Addition of NE to tissue culture medium or pretreatment of G-CSF with NE before its addition to media suppressed the growth of G-CSF-responsive cells. NE also cleaved the G-CSFR on the surface of intact cells resulting in a time-dependent reduction in cell surface expression of the G-CSFR. Notably, decreased G-CSFR surface expression resulting from treatment of cells with NE was also associated with a reduction in cell viability and proliferation in response to G-CSF. These results are the first to demonstrate that G-CSF and G-CSFR are proteolytically cleaved by NE and that NE-induced degradation of these proteins correlates with a reduction in the biologic activity of the cytokine and a decrease in the signaling function of the receptor because of decreased G-CSFR surface expression. These findings provide additional insights into mechanisms by which G-CSF/G-CSFR interactions may be modulated.     

A randomized comparison of once versus twice daily recombinant human granulocyte colony-stimulating factor (filgrastim) for stem cell mobilization in healthy donors for allogeneic transplantation

To evaluate the schedule dependency of granulocyte colony-stimulating factor (G-CSF) (filgrastim) for stem cell mobilization, we conducted a randomized comparison in 50 healthy donors, with one subcutaneous daily injection of 10 microg/kg G-CSF (n = 25) compared with twice injections daily of 5 microg/kg G-CSF (n = 25). The two groups were well balanced for age, body weight and sex. G-CSF application was performed on an out-patient basis and leukapheresis was started in all donors on day 5. The most frequent side-effects of G-CSF were mild to moderate bone pain (88%), mild headache (72%), mild fatigue (48-60%) and nausea (8%) without differences between the two groups. The CD34(+) cell count in the first apheresis was 5.4 x 10(6)/kg donor weight (range 2.8-13.3) in the 2 x 5 microg/kg group compared with 4.0 x 10(6)/kg (range 0.4-8.8) in the 1 x 10 microg/kg group (P = 0.007). The target of collecting > 3.0 x 10(6) CD34(+) cells/kg donor weight with one apheresis procedure was achieved in 24/25 (96%) donors in the 2 x 5 microg/kg group and in 17/25 (68%) donors in the 1 x 10 microg/kg group. The target of collecting > 5.0 x 10(6) CD34(+) cells/kg in the first apheresis was achieved in 64% in the 2 x 5 microg/kg group, but in only 36% in the 1 x 10 microg/kg group. The progenitor cell assay for granulocyte-macrophage colony-forming units (CFU-GM) and erythroid burst-forming units (BFU-E) was higher in the 2 x 5 microg/kg group than in the 1 x 10 microg/kg group (7.0 vs. 3.5 x 10(5)/kg, P = 0.01; 6.6 vs. 5.0 x 10(5)/kg; P = 0.1). Administering G-CSF (filgrastim) at a dosage of 5 microg/kg twice daily rather than 10 microg/kg once daily is recommended; this leads to a higher CD34(+) cell yield and requires fewer apheresis procedures without increasing toxicity or cost.     

支气管哮喘患者外周血中的CD+4 CD+25 T淋巴细胞的测定

目的阐明支气管哮喘(简称哮喘)患者外周血中是否存訡D+4 CD+25 T调节性淋巴细胞,并探讨CD+4 CD+25细胞的免疫抑制活性.方法应用流式细胞仪检测29例过敏性哮喘患者[急性发作期患者(急性发作期)15例、缓解期患者(缓解期)14例和16名非过敏性健康志愿者(正常对照组)外周血中CD+4 CD+25 细胞数量变化.应用免疫磁珠法分离提纯CD+4 CD+25 细胞,将纯化的CD+4 CD+25细胞和(或)CD+4 CD-25细胞在体外培养,观察CD+4 CD-25细胞的增殖反应,将收集培养的上清液用酶联免疫吸附测定(ELISA)法检测Th1类细胞因子γ干扰素(IFN-γ)和Th2类细胞因子白细胞介素4(IL-4)和IL-13.结果急性发作期患者外周血中CD+4 CD+25细胞比值为(14.9±1.8)%,缓解期患者为(11.8±0.7)%,正常对照组为(11.2±0.8)%,发作期与缓解期患者比较差异有统计学意义(P<0.01);缓解期患者与正常对照组比较差异无统计学意义(P>0.05).哮喘组CD+4 CD-25细胞增殖反应为(74±9)%,正常对照组为(72±8)%,两组比较差异无统计学意义(P>0.05).此外,哮喘组和正常对照组的CD+4 CD+25 细胞均能抑制CD+4 CD-25细胞产生IFN-γ、IL-4和IL-13,而且两组的抑制能力也无明显区别.结论急性发作期哮喘患者外周血CD+4 CD+25 细胞数明显高于缓解期患者和正常对照组.哮喘患者的CD+4 CD+25 细胞的抑制活性和正常对照组比较差异无统计学意义.谮     

Proliferation and differentiation of myelodysplastic CD34+ cells: phenotypic subpopulations of marrow CD34+ cells

In a search for a mechanism to explain the impaired growth of progenitor cells in patients with myelodysplastic syndromes (MDS), marrow CD34+ cells were purified up to 94.9% +/- 4.2% for normal individuals and 88.1% +/- 17.6% for MDS patients, using monoclonal antibodies and immunomagnetic microspheres (MDS CD34+ cells). Phenotypic subpopulations of these CD34+ cells were analyzed for CD38, HLA-DR, CD33, CD13, CD14, CD41 and CD3 plus CD19, in association with proliferative and differentiative capacities. The 15 studies performed included 12 MDS patients. Coexpression rate of CD13 significantly increased in the MDS CD34+ cell population with a value of 91.4% +/- 11.6% and ranging from 60.3% to 100%, and exceeded 99% in four studies, whereas that of normal CD34+ cells was 49.9% +/- 15.8%, ranging from 28.2% to 70.1% (P < .001). Coexpression rate of CD38, HLA-DR, CD33, CD14, and CD3 plus CD19 in MDS CD34+ cells did not significantly differ from that of normal CD34+ cells. The total number of colonies and clusters grown from 100 normal marrow CD34+ cells was 40.4 +/- 8.6, the range being from 27.2 to 50.3; this varied in MDS marrow CD34+ cells with a value of 34.0 +/- 28.7, the range being 0 to 95.9. The lineage of colonies and clusters promoted by MDS marrow CD34+ cells was predominantly committed to nonerythroid with impaired differentiation in 13 of 15 studies (87%). CD13 is first expressed during hematopoiesis by colony-forming unit granulocyte-macrophage and is absent in erythroid progenitors. Therefore, this study provides direct evidence for the lineage commitment of MDS CD34+ cells to nonerythroid with impaired differentiation and explains the mechanism of nil or low colony expression of MDS progenitor cells to erythroid lineage.     

Expression and prognostic significance of Bcl-2 family proteins in myelodysplastic syndromes

Excessive apoptosis is implicated in the pathogenesis of myelodysplastic syndromes (MDS). We assessed by flow cytometry the expression of several members of the Bcl-2 family in bone marrow mononuclear cells (BMMNC) of 168 MDS samples at diagnosis. The proteins studied were Bcl-2, Bcl-xL (anti-apoptotic), Bax, Bad, Bak, and Bcl-xS (pro-apoptotic). The percentage of BMMNC expressing Bcl-2 and Bcl-xL was higher in refractory anemia with excess of blasts (RAEB), RAEB in transformation (RAEB-T), and chronic myelomonocytic leukemia (CMML) than in refractory anemia (RA) and RA with ringed sideroblasts (RAS). Conversely pro-apoptotic proteins Bad, Bak, and Bcl-xS were detected in a higher percentage of cells in RA and RAS. RA and RAS were associated with an increased Bcl-xS/Bcl-xL ratio. The expression of anti-apoptotic proteins was also correlated with that of CD34 and P170 and with the percentage of blast cells. Two-color analyses demonstrated that CD34 and Bcl-2 were usually expressed in the same cells. No significant correlation was found with cytogenetic abnormalities. Higher expression of pro-apoptotic Bcl-2-family proteins (Bak, Bad, Bcl-xS) and higher Bcl-xS/Bcl-xL ratio were associated with longer survival and decreased risk of leukemic transformation in univariate analysis, whereas expression of anti-apoptotic proteins was associated with decreased survival. Consequently Bcl-2 proteins expression was well correlated with the International Prognostic Scoring System (IPSS). Our data confirm that the control of apoptosis is deregulated in MDS cells. Moreover, the study of markers such as CD34 (or Bcl-2), Bcl-xL, and Bcl-xS provides additional prognostic information.     

CD+8CD-28T淋巴细胞在肺结核发病机制中的作用

目的 探讨CD8^＋CD28^-T淋巴细胞在肺结核发病机制中的作用。方法 30例病例为2005年3月至5月遵义医学院附属医院呼吸内科住院及门诊患者，采用流式细胞术检测15例肺结核组患者外周血中CD8^＋CD28^-T淋巴细胞比值、细胞内白细胞介素6（IL-6）水平，以及CD3^＋、CD3^＋CD8^＋、CD8^CD28^＋T淋巴细胞比值，15例慢性支气管炎急性发作期患者作为疾病对照组，15名健康人作为健康对照组。结果 肺结核组和疾病对照组CD3^＋T淋巴细胞分别为（41±16）％和（40±10）％，均显著低于健康对照组[（44±6）％]；肺结核组和疾病对照组CD8^＋CD28^＋T淋巴细胞[（47±16）％和（44±10）％]均显著高于健康对照组[（41±12）％]；肺结核组CD8^＋CD28^＋T淋巴细胞[（15±8）％]显著低于疾病对照组[（20±7）％]，两组均显著低于健康对照组[（32±9）％]；肺结核组CD8^＋CD28^-T淋巴细胞[（27±9）％]显著高于疾病对照组[（22±9）％]，两组均显著高于健康对照组[（10±4）％]；肺结核组CD8^＋CD28^-T淋巴细胞分泌的IL-6水平[（32．4±2．4）％]显著高于疾病对照组和健康对照组[（19．7±3．2）％和（15．2±2．7）％]。结论 肺结核患者CD8^＋CD28^-T淋巴细胞及其分泌的IL-6水平在外周血中上调，CD8^＋CD28^＋T淋巴细胞水平在外周血中下调。CD8^＋CD28^＋和CD8^＋CD28^-T淋巴细胞及其分泌的IL-6可能参与肺结核的发病机制。CD8^＋CD28^＋未和CD8^＋CD28^-T淋巴细胞比值及其分泌的IL-6水平可作为活动性肺结核的辅助诊断指标。     

外周血CD+4CD+25T细胞表达在系统性红斑狼疮患者中的意义

目的了解系统性红斑狼疮(SLE)患者外周血CD4 CD2 5T细胞表达及其临床意义。方法用流式细胞仪检测53例SLE患者外周血CD4 CD2 5T细胞表达,根据CD25表达荧光强度>100者为CD4 CD25brightT细胞,并与SLE活动指数评分(SLEDAI)、血清补体C3水平、抗双链DNA抗体、抗核抗体滴度进行相关分析。结果SLE患者外周血CD4 CD2 5T细胞表达率为(7·84±1·85)%,显著低于对照组(9·18±2·01)%(P<0·05),且活动期组[(6·72±1·16)%]较稳定期组更低[(8·57±1·91)%,P<0·01]。外周血CD4 CD25brightT细胞表达率在活动期组[(0·85±0·24)%]和稳定期组[(0·91±0·25)%]之间相比差异无统计学意义(P=0·686),但均低于对照组[(1·43±1·08)%,P<0·01]。随治疗后SLEDAI评分的下降,活动期组SLE患者外周血CD4 CD25brightT细胞表达率无明显变化。进一步分析外周血CD4 CD25brightT细胞表达率与SLEDAI评分、抗核抗体、抗双链DNA抗体滴度和血清C3水平的相关性,分别为ρ=-0·188,P=0·178;ρ=-0·216,P=0·121;ρ=0·082,P=0·560;ρ=0·010,P=0·944,差异均无统计学意义(P>0·05)。结论外周血CD4 CD2 5T细胞的减少可能与SLE的发病有关。