Acute exercise and T-lymphocyte expression of the early activation marker CD69

PURPOSE: This study aimed to determine the effect of acute exercise on the proliferation and expression of activation markers on T-lymphocytes. METHODS: Seventeen well-trained male endurance runners completed 60 min of treadmill running at 95% of ventilatory threshold and a resting, no exercise, control session at the same time of day. Five blood samples were collected at each session: before exercise, mid-exercise, immediately after exercise, and 30 min and 60 min after exercise. Isolated peripheral blood mononuclear cells (PBMC) were stimulated with the mitogen PHA. Activation was measured using the expression of CD69 (assessed by three-color flow-cytometry), and cellular proliferation was assessed using 3-(4,5-dimethlthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) dye uptake. RESULTS: At all sampling points, there was a significant difference (P < 0.05) in the percentage of CD4 and CD8 cells that became activated (CD69+) after mitogen stimulation (68% of CD4 compared with 45% of CD8 cells). Exercise had no effect on the percentage of cells that became activated in response to mitogen. There was a significant exercise-induced decrease in lymphocyte proliferation of PBMC, but when expressed per-T-cell (CD3+), there was no difference between the exercise and control condition. CONCLUSION: This study indicated that on an individual cell basis 1 h of exercise at 95% of ventilatory threshold did not alter the ability of T-lymphocytes (CD3+) or T-lymphocyte subsets (CD3+CD4+ and CD3+CD8+) to become activated and did not alter the ability of T-lymphocytes to proliferate.     

Memory CD4 T-cell subsets discriminated by CD43 expression level in A-bomb survivors

Purpose:?Our previous study showed that radiation exposure reduced the diversity of repertoires of memory thymus-derived cells (T cells) with cluster of differentiation (CD)- 4 among atomic-bomb (A-bomb) survivors. To evaluate the maintenance of T-cell memory within A-bomb survivors 60 years after radiation exposure, we examined functionally distinct memory CD4 T-cell subsets in the peripheral blood lymphocytes of the survivors.

Methods:?Three functionally different subsets of memory CD4 T cells were identified by differential CD43 expression levels and measured using flow cytometry. These subsets consist of functionally mature memory cells, cells weakly responsive to antigenic stimulation, and those cells functionally anergic and prone to spontaneous apoptosis.

Results:?The percentages of these subsets within the peripheral blood CD4 T-cell pool all significantly increased with age. Percentages of functionally weak and anergic subsets were also found to increase with radiation dose, fitting to a log linear model. Within the memory CD4 T-cell pool, however, there was an inverse association between radiation dose and the percentage of functionally mature memory cells.

Conclusion:?These results suggest that the steady state of T cell memory, which is regulated by cell activation and/or cell survival processes in subsets, may have been perturbed by prior radiation exposure among A-bomb survivors.     

Low dose radiation induced immunomodulation: Effect on macrophages and CD8+ T cells

Purpose: The aim of the present investigation was to study the effect of fractionated whole body low dose ionizing radiation (LDR) on the functional responses of T lymphocytes, their subpopulations and macrophages.

Materials and methods: C57BL/6 mice were exposed to 4 cGy from a ⁶⁰Co source, at 0.31 cGy/min, at 24 h intervals for 5 days (total dose 20 cGy). Phagocytic activity was measured by flow cytometry using Bioparticles® and nitric oxide generation was estimated by spectrophotometry. Proliferation of lymphocytes in response to concanavalin A (con A) and alloantigens was measured by ³H thymidine incorporation. Expression of cell surface markers was assessed by flow cytometric analysis of antibody labeled cells. Target cell killing by cytotoxic T cells (CTL) generated against allogenic cells was assessed by flow cytometry using PKH26 labeled target cells. Cytokines were estimated by enzyme linked immunosorbent assay.

Results: Exposure to LDR enhanced nitric oxide secretion and phagocytosis. The expression of early activation antigen, CD69, was enhanced in CD8⁺ T lymphocytes concomitant with enhanced proliferation in response to con A. In addition, mixed lymphocyte reaction (MLR) and CTL response were augmented and secretion of interferon gamma (IFN-γ) was suppressed following LDR exposure.

Conclusions: LDR exposure enhanced the function of macrophages and responses of CD8⁺ T cells in C57BL/6 mice.     

Low dose radiation induced immunomodulation: effect on macrophages and CD8+ T cells

PURPOSE: The aim of the present investigation was to study the effect of fractionated whole body low dose ionizing radiation (LDR) on the functional responses of T lymphocytes, their subpopulations and macrophages. MATERIALS AND METHODS: C57BL/6 mice were exposed to 4 cGy from a (60)Co source, at 0.31 cGy/min, at 24 h intervals for 5 days (total dose 20 cGy). Phagocytic activity was measured by flow cytometry using Bioparticles and nitric oxide generation was estimated by spectrophotometry. Proliferation of lymphocytes in response to concanavalin A (con A) and alloantigens was measured by (3)H thymidine incorporation. Expression of cell surface markers was assessed by flow cytometric analysis of antibody labeled cells. Target cell killing by cytotoxic T cells (CTL) generated against allogenic cells was assessed by flow cytometry using PKH26 labeled target cells. Cytokines were estimated by enzyme linked immunosorbent assay. RESULTS: Exposure to LDR enhanced nitric oxide secretion and phagocytosis. The expression of early activation antigen, CD69, was enhanced in CD8(+) T lymphocytes concomitant with enhanced proliferation in response to con A. In addition, mixed lymphocyte reaction (MLR) and CTL response were augmented and secretion of interferon gamma (IFN-gamma) was suppressed following LDR exposure. CONCLUSIONS: LDR exposure enhanced the function of macrophages and responses of CD8(+) T cells in C57BL/6 mice.     

Static magnetic fields generated by a 0.5 T MRI unit affects in vitro expression of activation markers and interleukin release in human peripheral blood mononuclear cells (PBMC).

PURPOSE: To investigate the effects of the static magnetic field (SMF) generated by a 0.5 T superconducting MRI unit on in vitro activation marker expression and interleukin release in human peripheral blood mononuclear cell (PBMC) samples from healthy volunteers. MATERIALS AND METHODS: PBMC samples were split into two groups: exposed and sham-exposed under isothermal conditions. PBMC were exposed for 2 h at 24 degrees C to the SMF of a 0.5 T superconducting MRI unit. Immediately after exposure, both samples were cultured for 24 h at 37 degrees C with or without mitogenic stimulation by phytohaemagglutinin (PHA). PBMC were examined for expression of CD25, CD69 and CD71 by immunofluorescence analysis and supernatants were assayed to quantify IFN-gamma, TNF-alpha and IL-4 by ELISA. RESULTS: The 0.5 T SMF produced, after 24 h of culture, a reduced expression of CD69 from PBMC in vitro, that was enhanced after PHA stimulation. An increased release of IFN-gamma and IL-4 was also found, which was reduced after PHA stimulation. The release of TNF-alpha, IL-6 and IL-10 was not modified. CONCLUSIONS: The SMF generated by a 0.5 T superconducting MRI unit modified in vitro activation marker expression and interleukin release from human PBMC.     

Post-mortem markers of sepsis: an immunohistochemical study using VLA-4 (CD49d/CD29) and ICAM-1 (CD54) for the detection of sepsis-induced lung injury

The up-regulation of different adhesion molecules such as VLA-4 (CD49d/CD29) and ICAM-1 (CD54) on the pulmonary endothelium and leukocytes, is a key event in sepsis-induced lung injury leading to inflammatory tissue alterations. The value of VLA-4 and ICAM-1 as micromorphological post-mortem markers for the detection of sepsis-induced lung injury, was evaluated in a semiquantitative immunohistochemical study. VLA-4 was strongly expressed on intravascular, interstitial and intra-alveolar leukocytes in sepsis-associated fatalities, whereas in non-septic fatalities an irregular weak immunoreactivity was observed on interstitial leukocytes and no positive immunohistochemical expression was detected on intravascular or intra-alveolar leukocytes. ICAM-1 was strongly expressed on endothelial cells of the pulmonary microvasculature and on pulmonary macrophages and lymphocytes in sepsis-associated fatalities. In contrast, an infrequent weak immunohistochemical reaction for ICAM-1 was found on pulmonary endothelium and on perivascular leukocytes in non-septic fatalities. Based on the results of the present preliminary study, VLA-4 and ICAM-1 can be considered as useful immunohistochemical post-mortem markers of sepsis. Received: 28 February 2000 / Accepted: 22 May 2000     

再生障碍性贫血患者T淋巴细胞早期激活功能的研究

目的:了解再生障碍性贫血(AA)患者T淋巴细胞早期激活功能的变化。方法:应用流式细胞仪分析了34例AA患者骨髓和外周血单个核细胞T淋巴细胞亚群的变化以及CD4 和CD8 T细胞培养前后CD69的表达情况。结果:AA患者存在T细胞亚群数量的异常,CD4 /CD8 比值的下降与对照组比较有显著差异。重症AA患者体内有一部分CD4 与CD8 细胞表达CD69,而慢性AA患者只有部分CD8 细胞表达CD69,应用PHA刺激T细胞4 h后,AA和正常对照CD4 与CD8 T细胞CD69的表达率均迅速升高,但重症AA和慢性AA患者CD69的表达率均显著高于正常对照。结论:AA患者不仅存在T细胞数量异常,而且其T细胞早期激活功能也异常,可能与AA发病机制有关。     

Expression of lymphocyte subsets after exercise and dexamethasone in high and low stress responders

PURPOSE: Recent work indicates that among the normal population, persons can be classified as low (LR) or high (HR) stress responders based on hypothalamic-pituitary-adrenal (HPA) axis responses to high-intensity exercise. We studied whether differential activation of the HPA axis affected cytokine production and expression of selected lymphocyte subsets in HR and LR in response to high-intensity exercise after placebo and dexamethasone (DEX; 4 mg). METHODS: Healthy HR (N = 12) and LR (N = 10) underwent two exercise tests at 90% of VO2max, 8 h after placebo or DEX. Expression of lymphocyte surface markers (CD3+, CD4+, CD8+, CD56+), adhesion molecule markers (intercellular adhesion molecule-1/ICAM-1: CD54+ and L-selectin: CD62L+), and concentrations of plasma interleukin 6 (IL-6) were examined before and after exercise. RESULTS: Baseline percentages of CD8+ and CD56+ cells were significantly higher, and concentrations of IL-6 and percentages of CD4+ cells were significantly lower in HR as compared with LR. The percentage of CD54+ and CD62L+ cells was not significantly different in HR and LR. DEX significantly reduced the percentage of CD3+ and CD4+ and increased the percentage of CD8+ and CD56+ subsets; the percent of cells expressing CD54+ increased, whereas CD62L+ decreased. Exercise-induced changes in the percentage of lymphocyte subsets were similar to those induced by DEX. CONCLUSION: In summary, HR and LR have different baseline patterns of IL-6 and lymphocyte subsets, which may reflect differential sensitivity to endogenous glucocorticoids. However, exogenous glucocorticoids induced similar patterns of lymphocyte expression in HR and LR.     

Sensorimotor performance and computational demand during short-term exposure to microgravity

INTRODUCTION: Previous research suggests that human sensorimotor performance depends both on task difficulty, and on the allocation of the brain's computational resources to the task. We employ this view to analyze the changes of sensorimotor performance during the microgravity episodes of parabolic flight. METHODS: There were seven subjects who participated before, during, and after exposure to the microgravity episodes of parabolic flight. They performed a tracking task with one hand, and a four-choice reaction time task with the other hand, either alone or concurrently. Overall performance scores across tasks were calculated. RESULTS: Overall single-task performance deteriorated by about 50% microgravity, with little sign of recovery during the flight. Overall dual-task interference was more than twice as great at the onset of microgravity than at the onset of the 1-G baseline, but converged toward that baseline within about 4.5 min. CONCLUSIONS: Our subjects accepted a consistently poor level of sensorimotor performance throughout exposure to microgravity. To maintain that level, they increased the allocation of computational resources to the tasks at the onset of microgravity, but an increase was no longer necessary after 4.5 min of microgravity exposure. We take the initial increase as evidence of a brief phase of sensorimotor adaptation.     

Amifostine enhances recovery and expansion of peripheral FAS/CD95+ T- and NK-cell subpopulations during radiotherapy of patients with head-neck cancer

Purpose:?Experimental studies suggest that the FAS/APO-1/CD95 (cytokine receptor protein TNF-receptor superfamily, member 6) cell surface molecule is involved in the apoptotic effect of radiotherapy. In this study we investigated the role of amifostine in protecting the CD95+ (CD: cluster of differentiation) lymphocytic subpopulation in patients with head and neck cancer undergoing radiotherapy.

Materials and methods:?Using flow-cytometry we examined the expression of FAS/CD95 antigen on CD4+ (helper/inducer T cells), CD8+ (suppressor/cytotoxic T cells) and CD56+ (NK, natural killer) T-lymphocytes of 28 patients with head and neck cancer undergoing radiotherapy (with and without amifostine).

Results:?The numbers of peripheral blood lymphocytes were significantly reduced after treatment from (mean value ± STD error) 1477 ± 129 to 1015 ± 77 for T lymphocytes, 700 ± 70 to 454 ± 38 for CD4, 449 ± 46 to 296 ± 34 for CD8 and, 140 ± 18 to 118 ± 13 for NK, before and after treatment, respectively. CD95 expressing lymphocytes showed a faster recovery rate in patients receiving amifostine. CD95 expressing CD56 lymphocytes increased during radiotherapy in patients receiving daily cytoprotection with amifostine to values higher than the pre-treatment levels (p = 0.004).

Conclusion:?It is suggested that amifostine enhances recovery of T- and NK-lymphocyte subpopulations expressing the CD95 antigen in head-neck cancer patients undergoing RT and may enhance the efficacy of the later by interfering FAS-related immunological pathways.     

Substance P effects on developing thymocytes in hindlimb unloaded rats

INTRODUCTION: The purpose of this study was to examine the effects of substance P (SP) on the immune system in a condition similar to microgravity. We analyzed immune disturbances caused by subjecting Fischer 344 rats to a 45 degrees antiorthostatic suspension technique, otherwise known as the hindlimb unloading (HU) model. METHODS: Four groups of rats were assigned to either the prone control non-substance P group (P-NSP), prone control substance P group (P-SP), hindlimb unloaded non-substance P (HU-NSP) or the hindlimb unloaded substance P group (HU-SP). SP was administered at 10 ml of a 1 micromol x L(-1) concentration for 15 min x d(-1). HU and SP exposure for all groups lasted 16 d. After 16 d, 500 microl of blood was obtained to assay for both T-cell phenotype and corticosterone (CS) levels. Thymus lobes were excised in order to examine T-cell phenotype. Thymocytes were counted and stained for lymphocyte markers (CD4, CD8, and CD3). An analysis of variance (ANOVA) test was used to determine significance between groups (p < or = 0.05). RESULTS: HU-NSP rats showed a decrease in thymic CD4+CD8 +/- cells from 85.51 +/- 1.9% to 62.06 +/- 1.9% when compared with P-NSP rats. SP reversed these effects and returned CD4+CD8+ cells to control levels (76.60 +/- 1.9%). DISCUSSION: Daily SP treatment was found to reverse the deleterious effects caused by HU and corticosterone in rat thymic immune cells. SP could prove to be an effective means for keeping the immune system functioning at normal levels in microgravity, allowing astronauts to stay in space longer and maintain a more productive immune system.     

UVB-irradiated T-cells undergoing apoptosis lose L-selectin by metalloprotese-mediated shedding

PURPOSE: L-selectin (CD62L) is a prerequisite for leucocyte adhesion to endothelial cells of blood vessels and consequently for transmigration. Its expression on the cell surface therefore regulates the ability of lymphocytes to enter lymph nodes, to re-enter blood vessels or to invade tissues at sites of inflammation. The aim of this study was to determine the expression of CD62L on apoptotic lymphocytes after UVB irradiation. MATERIALS AND METHODS: Peripheral blood mononuclear cells (PBMC) were isolated from peripheral blood of normal healthy volunteers. Cells were stimulated with phorbol myristate acetate (PMA) and ionomycin for activation. Apoptosis in peripheral T-cells and Jurkat cells was induced by irradiation with UVB (120 mJ/cm2). In addition, T-cells or Jurkat cells were cultured for the indicated time with anti-Fas antibody CH11. The CH11-induced apoptosis was inhibited by the pan-caspase inhibitor zVAD-fmk. For detection of apoptosis, cells were analysed by cytofluorometry for morphological changes typical for apoptosis. The reliability of the apoptotic cell gate was confirmed by staining with FITC-labelled annexin-V in the presence ofpropidium iodide (PI). For FACS analysis of CD62L expression on the cell-surface immunofluorescence was performed using FITC-conjugated anti-CD62L and PE-conjugated anti-CD3 antibodies. Soluble CD62L (sCD62L) in the cell supernatants was measured by standard ELISA technique. Assays were performed in the presence and absence of metalloprotease inhibitor KB8301. RESULTS: PBMC from healthy volunteers undergoing apoptosis following UVB irradiation selectively shed CD62L, whereas the expression of the lineage-specific marker CD3 showed only minor changes. Shedding was blocked by the hydroxamic acid-based metalloprotease inhibitor KB8301. When Jurkat cells were treated with the caspase inhibitor zVAD-fmk, anti-CD95 antibodies did not induce apoptosis, and the expression of CD62L remained unaltered. CONCLUSION: UVB or ionizing radiation induce apoptosis in lymphocytes. The loss of CD62L is associated with apoptosis and will influence lymphocyte trafficking and, by excluding them from CD62L-mediated adhesion and tissue invasion, might contribute to the regulation of inflammation.     

A Clinical Study of Hypoxia Using Endogenous Hypoxic Markers and Polarographic Oxygen Electrodes

PURPOSE: To examine various kinds of endogenous hypoxia markers' expression in the tissues of uterine cervix cancer and to elucidate the characteristics and pitfalls when they are used as a hypoxia marker, by comparing these expressions with tumor oxygen partial pressure (pO2) values. PATIENTS AND METHODS: Assessment of pO2 using polarographic oxygen electrodes was performed in 69 patients with cervix carcinomas. Biopsies were taken from the region of electrode measurements. Expression of endogenous hypoxic markers in biopsy specimens such as vascular endothelial growth factor, glucose transporter-1 (GLUT-1), involucrin, and osteopontin was detected by immunohistochemistry. A double immunolabeling technique with GLUT-1 and MIB-1 as a marker of proliferation was also performed. RESULTS: There was no significant correlation between expression of endogenous hypoxic markers and pO2. The only significant association seen was between the fraction of necrosis and pO2. A significant but weak correlation was found among expression of endogenous hypoxic markers. The levels of necrosis were related negatively with levels of expression of endogenous hypoxic markers. The double immunolabeling technique with GLUT-1 and MIB-1 indicated that there were about 20% MIB-1-positive tumor cells without GLUT-1 expression in tissues adjacent to areas of necrosis. CONCLUSION: The existence of necrosis affected the expression of endogenous hypoxic markers. Some hypoxic tumor cells without expressions of hypoxia markers can maintain clonogenicity and influence the treatment results. The combined use of hypoxic markers is recommended because their expression is influenced by factors other than hypoxia.     

Mood change and immune status of human subjects in a 10-day confinement study

INTRODUCTION: Stress is a known factor that causes changes in leukocyte distribution or depression in lymphocyte proliferation. We reported previously that a 10-d confinement caused changes in immune status. Here we report the relationship between mood changes and immune parameters in the subjects confined for 10-d. METHODS: There were 10 subjects (age 20-27 yr, mean 22.8 yr) who participated in a 10-d confinement study. They were divided into 2 groups with regard to their psychological aspects and their immune parameters were then compared. Blood samples were taken once before, three times during, and once after confinement. The percentages of granulocytes, natural killer (NK) cells, and cells positive for CD69, an early activation marker, were analyzed by flow cytometry. Face scale was employed to estimate subjects' mood. RESULTS: The group that showed an increase in mood scale toward the end of the confinement showed changes in all immune parameters. In contrast, less marked changes were seen in the group that showed no mood changes throughout the experiment. DISCUSSION: These results indicate that the observed immune changes were related to the mood changes, and that mood change seems to be one of the causes of the immunological changes seen in confined environments, such as in space stations or submarines. The percentages of NK cells, granulocytes, and CD69 expression may be useful criteria for detecting immunological deterioration caused by stress, or for selecting astronauts who are immunologically stable against the challenge of confinement stress.     

Immune function in rats following repetitive exposures to 7 ATA air

INTRODUCTION: The precise action of the immunological effects associated with hyperbaric exposure is poorly understood. This study's goal was to clarify the effects and etiology of deep air dives on the immune response. METHODS: Sprague-Dawley rats were exposed to 7-ATA air for 60 min twice daily for 3 consecutive days. Several markers of immune function, the degree of stress, and oxidative stress following or during the exposures were determined. Rats exposed to 1.47-ATA oxygen or 7-ATA nitrox (0.21-ATA oxygen + 6.79-ATA nitrogen) were taken as controls. RESULTS: Peripheral lymphocytes and CD3+ and CD4+CD3+ subsets in peripheral blood and spleen, plasma interleukin-2 level, and the responses of splenic lymphocytes to concanavalin A all decreased, antioxidant enzyme activities and the concentration of reduced glutathione both decreased, while the level of malondialdehyde increased following hyperbaric air exposures. All changes returned to normal in 3-5 d. Similar changes were observed following exposures to 1.47-ATA oxygen, but not to normoxic nitrox. Plasma levels of adrenocorticotropic hormone and corticosterone increased after one exposure and recovered to normal levels after three exposures in rats treated with either hyperbaric or normobaric air. Pretreatment of the animals with N-acetylcysteine, a potent free radical scavenger and antioxidant attenuated the effects of hyperbaric air on immune and antioxidant systems. CONCLUSIONS: These results are consistent with the hypothesis that repetitive exposure to 7-ATA air has a temporary immunosuppressive effect on rats, which is related to oxidative stress induced by the high partial pressure of oxygen in breathing gas.     

Puberty effects on NK cell responses to exercise and carbohydrate intake in boys

Previous research has demonstrated that younger versus older animals and humans experience smaller perturbations in natural killer (NK) cells in response to physiological stress. PURPOSE: To determine whether the smaller perturbations in NK cells induced by strenuous exercise and carbohydrate (CHO) intake, previously reported in children, are influenced by puberty. METHODS: Twenty 12-yr-old boys, distinguished as prepubertal (Tanner (T) 1, N = 7), early pubertal (T2, N = 7), or pubertal (T3-5, N = 6), cycled for 60 min at 70% VO(2max) while drinking 6% CHO (CT) or flavored water (WT). Blood was collected at rest and during (30 and 60 min) and following (30 and 60 min) exercise to identify NK cells as CD3(-)CD56(dim) or CD3(-)CD56(dim). CD69 expression on CD3(-)CD56(+) cells was also determined. RESULTS: A puberty x CHO x exercise interaction was found for the proportion, but not number, of CD56(dim) cells (P = 0.06). CD56(dim) cell counts were lower in CT versus WT (P < 0.001). Responses of CD56(bright) proportions (P = 0.007) and counts (P = 0.03) depended on pubertal status, but not CHO. The CD56(bright):CD56(dim) ratio remained stable during exercise, but during recovery was higher in T1 and T3-5 versus T2 (P = 0.08) and in CT versus WT (P = 0.04). During recovery, CD3(-)CD56(+) cells expressed higher levels of CD69 (P = 0.01), with no change in the proportion of CD69(+) cells. CONCLUSION: These results confirm the influence of puberty on the distribution of NK cell subsets in response to exercise and CHO intake. Increased CD69 expression suggests that NK cells increase activation status during recovery from physiological stress.     

不明原因早期自然流产患者蜕膜淋巴细胞表面CD57的表达

以１０ 例正常妊早期行人工流产的健康孕妇作为对照组,采用间接免疫荧光标记及流式细胞计数的方法,对１０ 例不明原因早期自然流产患者蜕膜组织中淋巴细胞表面分化抗原ＣＤ５７ 的表达进行了检测。实验组与对照组相比,蜕膜淋巴细胞表面ＣＤ５７ 的表达显著升高,分别为２２ ．３８ ％ ±１ ．９８ ％ 、１８ ．９９％ ±１ ．８３ ％ （ Ｐ＜ ０ ．０００５） 。上述结果表明,患者蜕膜淋巴细胞表面ＣＤ５７ 的表达发生了改变,这为此种疾病的免疫学发病因素的探讨提供了一定的实验室参考依据。     

瘢痕疙瘩和增生性瘢痕病人细胞免疫的测定

目的：探讨细胞免疫与瘢痕增生的关系。方法：对6例瘢痕疙瘩,14例增生性瘢痕病人和10例正常人外周血淋巴细胞进行T淋巴细胞及其亚群分析和淋巴细胞试验。结果：瘢痕疙瘩和增生性瘢痕病人的外周血淋巴细胞中CD4^ ,CD4^ /CD8^ 及淋巴细胞转化率均高正常对照组。结论：T淋巴细胞免疫功能异常可能在瘢痕增生中起重要作用。     

早期梅毒皮损组织CD3、CD20和CD68的表达

为探讨一，二期梅毒皮损组织细胞免疫应答过程及机制，采用免疫组织化学及计算机图像分析的探讨，对一，二期梅毒病损组织中的CD3，CD20，CD68表达进行定性定量分析研究。结果显示，43例一，二期梅毒标本中CD3，CD20，CD68表达均阳性，表达水平病期发展，皮肤损害加重而逐渐升高。CD68表达水平高于CD3，CD20，尤其在血管周围表达明显增高，CD20表达较低。研究表明，T细胞，B细胞，特别是巨噬细胞在清除早期梅毒组织内感染的梅毒螺旋体过程中起着重要的细胞免疫调节作用，但作用不完全。     

UVB-irradiated T-cells undergoing apoptosis lose L-selectin by metalloprotease-mediated shedding

Abstract. Purpose : L-selectin (CD62L) is a prerequisite for leucocyte adhesion to endothelial cells of blood vessels and consequently for transmigration. Its expression on the cell surface therefore regulates the ability of lymphocytes to enter lymph nodes, to re-enter blood vessels or to invade tissues at sites of inflammation. The aim of this study was to determine the expression of CD62L on apoptotic lymphocytes after UVB irradiation. Materials and methods : Peripheral blood mononuclear cells (PBMC) were isolated from peripheral blood of normal healthy volunteers. Cells were stimulated with phorbol myristate acetate (PMA) and ionomycin for activation. Apoptosis in peripheral T-cells and Jurkat cells was induced by irradiation with UVB (120 mJ/cm2). In addition, T-cells or Jurkat cells were cultured for the indicated time with anti-Fas antibody CH11. The CH11-induced apoptosis was inhibited by the pan-caspase inhibitor zVAD-fmk. For detection of apoptosis, cells were analysed by cytofluorometry for morphological changes typical for apoptosis. The reliability of the apoptotic cell gate was confirmed by staining with FITClabelled annexin-V in the presence of propidium iodide (PI). For FACS analysis of CD62L expression on the cell-surface immunofluorescence was performed using FITC-conjugated anti-CD62L and PE-conjugated anti-CD3 antibodies. Soluble CD62L (sCD62L) in the cell supernatants was measured by standard ELISA technique. Assays were performed in the presence and absence of metalloprotease inhibitor KB8301. Results : PBMC from healthy volunteers undergoing apoptosis following UVB irradiation selectively shed CD62L, whereas the expression of the lineage-specific marker CD3 showed only minor changes. Shedding was blocked by the hydroxamic acid-based metalloprotease inhibitor KB8301. When Jurkat cells were treated with the caspase inhibitor zVAD-fmk, anti-CD95 antibodies did not induce apoptosis, and the expression of CD62L remained unaltered. Conclusion : UVB or ionizing radiation induce apoptosis in lymphocytes. The loss of CD62L is associated with apoptosis and will influence lymphocyte tra Ýcking and, by excluding them from CD62L-mediated adhesion and tissue invasion, might contribute to the regulation of inflammation.