IL—4对多发性骨髓瘤患者外周血细胞CD20及HLA—DR表达…

本文报道用流式细胞分析技术，检测了２８例多发性骨髓瘤（Ｍ Ｍ）患者和２０名健康对照者外周血Ｂ细胞（ＣＤ＾＋２０）以及Ｂ、Ｔ和单核细胞中ＨＬＡ－ＤＲ＾＋细胞比率。结果发现，ＭＭ患者ＣＤ＾＋２０以及Ｂ、Ｔ及单核细胞中ＨＬＡ－ＤＲ＾＋细胞比率与正常对照组差异非常显著（Ｐ＜０．０１）。加入重组ＩＬ－４，可使８名ＭＭ患者ＣＤ＾＋２０、ＨＬＡ－ＤＲ＾＋ＣＤ＾＋２０、ＨＬＡ－ＤＲ＾＋单核细胞比率提高非常显著（Ｐ     

智能低下患儿外周血T淋巴细胞亚群与sIL—2R水平的变化

本文检测５５例智能低下（ＭＲ）患儿及正常人外周血Ｔ淋巴细胞亚群及血清可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）的水平，结果表明ＭＲ患儿ＣＤ３＾＋、ＣＤ４＾＋细胞显著低于对照组，ＣＤ８＾＋细胞明显高于对照组，ＣＤ４＾＋／ＣＤ８＾＋比值下降。ｓＩＬ－２Ｒ活性明显高于对照组。     

慢性活动性乙型肝炎患者细胞免疫功能检测及其临床意义

测定了例慢性活动乙型肝炎患者外周血单个核细胞（ＰＢＭＣ）产生的白细胞介素２（ＩＬ－２）活性，其中部分病人检测了血清可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）水平，膜白细胞介素２受体（ｍＩＬ－２Ｒ）表达，ＬＡＫ活性及外周血Ｔ淋巴细胞亚群，并分析了它们之间的相关性，结果表明：ＩＬ－２活性，ｍＩＬ－２Ｒ表达，ＬＡＫ活性，ＣＤ４／ＣＤ８比值显著低于正常对照组（Ｐ〈０．００１），而ｓＩＬ－２Ｒ水平，ＣＤ８细胞显     

IL－4对多发性骨髓瘤患者外周血细胞CD20及HLA－DR表达的影响

本文报道用流式细胞分析技术，检测了２８例多发性骨髓瘤（ＭＭ）患者和２０名健康对照者外周血Ｂ细胞（ＣＤ２０＋）以及Ｂ、Ｔ和单核细胞中ＨＬＡ－ＤＲ＋细胞比率。结果发现，ＭＭ患者ＣＤ２０＋以及Ｂ、Ｔ及单核细胞中ＨＬＡ－ＤＲ＋细胞比率与正常对照组差异非常显著（Ｐ＜０．０１）。加入重组ＩＬ－４，可使８名ＭＭ患者ＣＤ２０＋、ＨＬＡ－ＤＲ＋ＣＤ２０＋、ＨＬＡ－ＤＲ＋单核细胞比率提高非常显著（Ｐ＜０．０１）。而在Ｔ细胞，Ｐ值则＞０．０５。我们认为由于ＩＬ－４分泌减少，一方面使多克隆Ｂ细胞激活及增殖受抑，另一方面使单核细胞ＨＬＡ－ＤＲ抗原表达减少，抗原提呈能力下降可能是ＭＭ发生多克隆免疫球蛋白抑制的重要原因。     

抗胸腺细胞球蛋白（ATG）对再生障碍性贫血患者淋巴细胞亚群的影响

利用ＡＰＡＡＰ桥联免疫酶标技术，对３６例接受ＡＴＧ治疗的再生障碍性贫血（ＡＡ）患者进行了淋巴细胞亚群检测，结果发现，ＡＡ患者外周血Ｔ淋巴细胞亚群ＣＤ＾＋３ＣＤ＾＋４细胞治疗前后无明显变化，但ＣＤ＾＋４／ＣＤ＾＋８比值，ＣＤ＾＋８细胞数目治疗前后却有显著性差异。ＡＡ患者外周血ＨＬＡ－ＤＲ＾＋细胞较正常明显增高，但ＡＴＧ治疗后却有所下降，本研究的结果表明，ＣＤ＾＋８，ＨＬＡＤＲ＾＋细胞增高及ＣＤ＾＋４     

呼吸道合胞病毒下呼吸道感染对机体细胞免疫的影响

为研究呼吸道合胞病毒（ＲＳＶ）急性下呼吸道感染（ＡＬＲＩ）的细胞免疫变化，对２５例病儿外周血白细胞介素２（ＩＬ－２）和可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）水平、Ｔ细胞白细胞介素２受体（ＩＬ－２Ｒ）表达率和Ｔ细胞亚群百分率进行检测。结果显示，急性期病儿外周血ＩＬ－２水平明显低于恢复期和正常对照组，Ｔ细胞ＩＬ－２Ｒ表达率亦明显降低，而ｓＩＬ－２Ｒ水平却显著增高。急性期病儿ＩＬ－２水平与Ｔ细胞ＩＬ－２Ｒ表达率和ＣＤ＋４细胞百分率呈正相关，与ｓＩＬ－２Ｒ水平和ＣＤ＋８细胞百分率呈负相关；ｓＩＬ－２Ｒ水平与Ｔ细胞ＩＬ－２Ｒ表达率呈负相关，与临床严重程度呈正相关。上述各项免疫指标异常均提示ＲＳＶ感染时机体存在细胞免疫功能紊乱。     

腺病毒、合胞病毒对外周血单个核细胞的IL-2受体表达及TNFα产生的影响

近年来国内外均注意到细胞因子及受体与病毒感染的关系。作者用１００ＴＣＩＤ５０的７型腺病毒（ＡＤＶ）及呼吸道合胞病毒（ＲＳＶ）Ｌｏｎｇ株刺激正常人体外培养的外周血淋巴细胞（ＰＢＭＣ），ＡＰＡＡＰ法检测淋巴细胞ＩＬ－２受体阳性率，酶联免疫法检测淋巴细胞上清液的ＴＮＦａ。初步观察了ＡＤＶ、ＲＳＶ对人ＰＢＭＣ的ＩＬ－２受体表达、ＴＮＦα产生的影响。经２００Ｕｇ／ｍｌ的ＰＨＡ活化的ＰＢＭＣ加入ＡＤＶ、ＲＳＶ后对照组ＩＬ－２＋细胞百分率为３４．３％，ＡＤＶ组为１７．３％，ＲＳＶ组为１７％，较对照组均显著降低…     

智能低下患儿外周血T淋巴细胞亚群与sIL－2R水平的变化

本文检测５５例智能低下（ＭＲ）患儿及正常人外周血Ｔ淋巴细胞亚群及血清可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）的水平，结果表明ＭＲ患儿ＣＤ３＋、ＣＤ４＋细胞显著低于对照组，ＣＤ８＋细胞明显高于对照组，ＣＤ４＋／ＣＤ８＋比值下降。ｓＩＬ－２Ｒ活性明显高于对照组。     

SLE患者AMLR与T细胞Ia抗原的改变及意义

本文以氚标胸腺嘧啶（＾３Ｈ－ＴｄＲ）掺入的淋巴细胞转化试验测定非Ｔ细胞刺激自身Ｔ细胞的增殖反应（ＡＭＬＲ）；用单克隆抗体（ＭｃＡｂ）Ｗｕ３５和Ｗｕ２２通过ＰＡＰ免疫酶标组化技术测定ＣＤ３＾＋，ＣＤ４＾＋，Ｃｄ８＾＋Ｔ细胞表面ＤＲ及ＤＱ抗原的表达。结果表明，活动期ＳＬＥ患者ＡＭＬＲ有明显减弱，Ｗｕ＾３５＋（ＨＬＡ－ＤＲ＾＋）Ｔ细胞增加为主，ＣＤ８＾＋ＤＲ＾＋及ＣＤ８＾＋ＤＱ＾＋细胞则表现为减少。提示     

胸腺肽治疗前后肝炎患者PBMC中mIL—2R^＋和HLA—DR^＋型细胞 …

用生物素－链霉亲和素系统免疫细胞化学检测了５０例慢性肝炎（ＣＨＢ）患者大剂量胸腺肽治疗前后ＰＢＭＣ中ｍＩＬ－２Ｒ＾＋细胞和ＨＬＡ－ＤＲ＾＋细胞数的变化动态。发现治疗３个月后,患者ｍＩＬ－２Ｒ＾＋细胞和ＨＬＡ－ＤＲ＾＋细胞占ＰＢＭＣ的百分率较治疗前有显著性增高,提示胸腺肽有增强淋巴细胞活性的功能,从一个侧面为胸腺肽治疗病毒性肝炎提供证据。     

CD4 T lymphocyte activation in acute severe asthma.

The expression of activation molecules on peripheral-blood CD4 and CD8 T lymphocytes and the serum concentrations of two products of activated T lymphocytes [interferon-gamma (IFN-gamma) and soluble interleukin-2 receptor (sIL-2R)] were measured in patients with acute severe asthma (ASA) and controls. Significantly higher percentages of CD4+ cells from patients with ASA expressed IL-2R, HLA-DR and VLA-1 as compared to controls (p less than 0.01). In contrast, CD8+ cells from both asthmatics and controls did not express IL-2R and VLA-1, and their expression of HLA-DR in asthmatics was not increased. Serum concentrations of IFN-gamma and sIL-2R were significantly elevated in patients with ASA as compared to control groups (p less than 0.01). Concentrations decreased as the patients improved clinically following therapy. Significant correlations were observed between the improvements in airways obstruction and (1) the decreases in the percentages of peripheral-blood IL-2R+ T lymphocytes and (2) the decreases in serum concentrations of sIL-2R. These observations suggest that CD4 T lymphocyte activation is important in the pathogenesis of ASA.     

T lymphocyte activation is associated with viral replication in chronic hepatitis B virus infection of childhood.

Activated circulating T lymphocytes expressing HLA-DR (mean +/- s.d. 11.0 +/- 5.2%) or interleukin-2 receptor (IL-2R) (2.1 +/- 1.7%) were significantly increased in 63 children with chronic hepatitis B virus (HBV) infection when compared with 33 age-matched healthy controls (3.0 +/- 1.3%, P less than 0.01, and 0.1 +/- 0.4%, P less than 0.01). HBeAg-positive patients had higher percentage of DR (11.9 +/- 5.1%) or IL-2R (2.4 +/- 1.7%) positive T lymphocytes than anti-HBe-positive children (7.4 +/- 3.6% and 1.1 +/- 1.5%, P less than 0.01 and P = 0.02 respectively). Similarly, HBV DNA-positive patients had higher percentage of DR (10.5 +/- 3.3) or IL-2R (3.2 +/- 1.7%) positive T cells than HBV DNA-negative children (6.6 +/- 2.8% and 1.2 +/- 1.5%, P less than 0.01 for both). There was a positive correlation between percentage of DR positive T lymphocytes and levels of HBV DNA. Sixty-two per cent of the DR-positive T lymphocytes were cytotoxic/suppressor and 35% helper/inducer. The relationship between viral replication and T lymphocyte activation is discussed.     

Elevation of activated gamma delta T cell receptor bearing T lymphocytes in patients with autoimmune chronic liver disease.

To study the possible role of T cells bearing the gamma delta T cell receptor (TCR) heterodimer in the pathogenesis of autoimmune chronic active hepatitis (AI-CAH) and primary sclerosing cholangitis (PSC) in children, we measured levels of gamma delta+ T cells in the peripheral blood, assessed the proportion of cells bearing the disulphide-linked (BB3+) and non-disulphide-linked (A13+) subtypes of the receptor, and studied the co-expression of TCR-gamma delta and the activation markers HLA-DR and IL-2 receptor (IL-2R), and the memory cell marker CD45RO. Percentage levels and absolute numbers of gamma delta +T cells were higher in both groups of patients than in controls (P less than 0.01), mainly as a result of an increase in both percentage levels and absolute numbers of the A13+ subtype (P less than 0.001). Co-expression of IL-2R and TCR-gamma delta was not found in controls but was present in some patients with AI-CAH (four out of 17) and PSC (six out of 12) at low levels (median 2.3%, range 1.7-5.0%). Expression of HLA-DR on gamma delta+ T cells was similar in both groups of patients and controls. The majority of gamma delta+ T cells in children with AI-CAH and PSC also expressed CD45RO (74.7 +/- 18.4% and 79.8 +/- 24.3%, respectively) at levels significantly higher than in controls (53.3 +/- 17.2%, P less than 0.01). These results suggest that autoimmune liver diseases in children are associated with an expansion and activation of gamma delta+ T cells in the peripheral blood, which may be important in the pathogenesis of these disorders.     

Assessment of selected co-stimulatory, adhesion and activatory molecules and cytokines of Th(1)/Th(2) balance in acute lymphoblastic leukemia in children

INTRODUCTION: Recent years have seen a rise in the importance of cytokine production and co-stimulatory/activatory molecule expression in the immune response in leukemia. The aim of our study was to assess the function of T lymphocytes in children with acute lymphoblastic leukemia (ALL) during remission induction based on selected cytokine and co-stimulatory/activatory molecule expression. MATERIAL/METHODS: The study group consisted of 50 children with ALL (B cell precursor). Peripheral blood samples were taken before treatment (day 0), after the prednisone prophase (day 8), and during (day 15) and after (day 33) remission induction. The percentages of T cells with interferon (IFN)-gamma (Th(1)), interleukin (IL)-4 (Th(2)) and IL-2 receptor (IL-2R), CD28, CTLA-4, CD38, ICAM-1, and HLA-DR expression were assessed by tricolor flow cytometry. RESULTS: At the time of diagnosis we noted higher percentages of T cells with adhesion molecule ICAM-1, activation molecule CD38 expression, and an increased population of Th(2 )cells (IL-4) compared with the control group. During and after remission induction we observed a decreased population of CD38(+) T cells, elevated percentages of helper T lymphocytes with IL-2R expression, and a rise in helper T lymphocytes producing IFN-gamma (Th(1)). During fever/infection, higher levels of activated T lymphocytes (CD4(+)HLA-DR(+), CD8(+)HLA-DR(+)), a rise in Th1, and no change in Th(2 )populations were observed. CONCLUSIONS: The results suggest T cell activation and Th(2 )predominance at the time of diagnosis and during remission induction in ALL in children. These results confirm the involvement of cellular immunity in the leukemic process and can be used in immune therapy in leukemia.     

Expression of p75 chain of IL-2 receptor in the early immunological reconstitution after allogeneic bone marrow transplantation.

Expression of p55 and p75 chains of IL-2 receptor (IL-2R) on the surface of both T and natural killer (NK) circulating lymphocytes was investigated in 14 paediatric patients given allogeneic bone marrow transplantation (BMT) from HLA-identical sibling or partially matched family donors. IL-2-induced proliferative and cytotoxic responses were also studied and all analysis was performed within 45 days from transplant. We found that, early after transplant, the percentage of p55+ and of p75+ peripheral blood lymphocytes (PBL) was not significantly different in patients who had received HLA-identical BMT (p55+ 8.04 +/- 4.87%; p75+ 28.27 +/- 18.85%) compared with healthy controls (p55+ 7.26 +/- 6.17%; p75+ 19.42 +/- 10.49%), while recipients of T cell-depleted marrow included a remarkably high percentage (76-90%) of p75+ PBL, which were mostly CD3- and co-expressed CD56 molecule. Comparable values of p55+ lymphocytes were observed in all patients and controls. However, in contrast to the other two groups, in recipients of T cell-depleted BMT the majority of these cells co-expressed p75 chain and CD56 antigen. IL-2-induced proliferation and lymphokine-activated killer (LAK) activity were detectable in all patients, and their values did not correlate with expression of p55 or p75 chains. Our data suggest that expansion of NK subsets expressing IL-2R chains after T cell-depleted BMT may be related to early reconstitution of natural immunity in the presence of allogeneic stimuli.     

Impaired generation of high-affinity interleukin-2 receptors in the autologous mixed lymphocyte reaction in rheumatoid arthritis.

We examined the expression of high-affinity interleukin (IL)-2 receptors (IL-2R) as well as Tac and HLA-DR antigens on peripheral blood (PB) T cells from 11 rheumatoid arthritis (RA) patients and 8 healthy controls induced in the autologous mixed lymphocyte reaction (AMLR). The proportion of HLA-DR- and Tac-bearing T cells and expression of these activation antigens were higher in patients relative to controls (P less than 0.01) in freshly isolated unstimulated PB mononuclear cells. AMLR stimulation of RA T cells failed to induce an increase in the proportion of HLA-DR and Tac-bearing T cells which was observed in health controls. After AMLR stimulation the number of high-affinity IL-2R were significantly lower in RA patients compared with controls (P less than 0.01). The number of high-affinity IL-2R on patient T cells correlated strongly with AMLR reactivity as measured by [3H]thymidine incorporation (r = 0.821, P = 0.002). The results suggest that the AMLR defect in RA may result from impaired generation of high-affinity IL-2R.     

蚕蚀性角膜溃疡患者外周血淋巴细胞免疫表型和T细胞活化的研究

目的：观察蚕蚀性角膜溃疡患者外周血淋巴细胞免疫表到和T细胞活化的变化,进一步探讨本病患者的免疫功能。方法：用流式细胞术检测8例活动性蚕蚀性角膜溃病患者外周血淋巴细胞对项免疫表型变化,用植物凝集素和沸被醉酯作为刺激剂,以HLA－DR,CD69、CD71、CD25的表达为T细胞活化的指标,用流式细胞术分析。结果：蚕蚀性角膜溃疡患者外周血CD4、CD5、CD8、CD10、CD11b、CD15、CD16、CD19、CD23、CD25、CD41、CD69、HLA-DP、HLADR抗原表达阳性淋巴细胞以及HLA－DR、CD69、CD71、CD25在CD3和CD8细胞的表达均明显高于正常对照组。结论：蚕蚀性角膜溃疡患者具有增强的细胞免疫和体液免疫,外周血T细胞及其亚群出现异常活化,反映患者体内存在自身免疫反应而支持该病发病之自身免疫学说。     

Activation of the immune system of cancer patients by continuous i.v. recombinant IL-2 (rIL-2) therapy is dependent on dose and schedule of rIL-2.

The effect of dose and schedule of continuous i.v. rIL-2 infusions on leucocyte subset counts, activation status of CD56+CD3- natural killer (NK) and CD3+ T lymphocytes, and cytolytic activities of peripheral blood mononuclear cells (PBMC) was studied. A single 4-day course of rIL-2 in escalating doses (0.9-11.5 x 10(6) U/m2 per day) was given to 18 patients with various types of metastatic cancer. The serum IL-2 concentration during rIL-2 therapy ranged between 23 and 64 U/ml and was proportional to the administered rIL-2 dose, as was the rebound lymphocytosis following therapy. Before therapy, the CD56+CD3- NK cells expressed low levels of the p75 chain of the IL-2 receptor (IL-2R) and virtually no IL-2R(p55). Most CD3+ T cells were IL-2R(p55-,p75-). Between 2 and 4 days following therapy, i.e. at the time of lymphocytosis, the percentage of CD56+,CD3- NK cells among the lymphocytes had increased proportional to the administered rIL-2 dose. The levels of IL-2R(p75) expression by the CD56+,CD3- NK cells had increased. The percentages of CD3+ T cells expressing IL-2R(p55), HLA-DR and CD45RO had increased proportional to the administered rIL-2 dose. The level of lymphokine- activated killer (LAK) activity against Daudi cells was also positively correlated with rIL-2 dose. Subsequently, seven patients received 4-weekly cycles of rIL-2 (2.9-4.4 x 10(6) U/m2 per day) during 4 consecutive weeks. This schedule led to marked increments in lymphocyte and eosinophil counts, and to increased cytolytic activities compared with pretreatment. We conclude that CD56+,CD3- NK and CD3+ T cells are activated differentially by continuous i.v. rIL-2 proportional to dose and duration of treatment.     

Immune activation and T cell subset abnormalities in circulation of patients with recently diagnosed type I diabetes mellitus.

The peripheral blood lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM) and healthy controls were analysed for the HLA-DR+, interleukin-2 receptor-positive (IL-2R+) activating antigens, and for CD45R+ and CDw29+ subsets from the purified CD4+ and CD8+ T cells populations. Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. However, the percentage of CD4+ CD45R+ suppressor/inducer T cells were decreased and CD4+ CDw29+ helper/inducer T cells increased in all patients with IDDM, compared with healthy controls. Thus, IDDM patients exhibit a deficiency in the CD4+ CD45R+ suppressor/inducer T cell subsets, which is probably related to the autoimmune phenomenon in this disease. In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. An alteration in the CD4+ CD45R+ and CD4+ CDw29+ T cell subsets appears to be a characteristic feature, and may relate to the impaired cell-mediated immunity in IDDM. These data provide new evidence for T cell dysregulation in IDDM.