Lymphocyte subsets of the peripheral blood in Sj?gren's syndrome and rheumatoid arthritis

Lymphocyte subsets were determined in the peripheral blood from twenty-three patients with primary Sj?gren's syndrome (SS) and sixteen patients with clinically active rheumatoid arthritis (RA) by two-color flowcytometry using various monoclonal antibodies. In both diseases, T-cells (CD3+), suppressor/cytotoxic cells (CD8+) and their cytotoxic subset (CD8+CD11-) were decreased, as compared with thirty-one healthy controls. B-cells (CD 21+ and CD 3-DR+) and activated T-cells (CD 3+DR+) were increased in SS patients. Helper T-cells (CD 4+Leu8-), suppressor-inducer T-cells (CD4+Leu8+), suppressor T-cells (CD8+Leu 15+) and three natural killer (NK) cell subsets determined by both CD16 and Leu7 antibodies did not differ between controls and SS or RA, although Leu7+NK cells were significantly increased in SS patients. In addition, we found that the treatment with low-dose prednisolone decreased B-cells and suppressor-inducer T cells, and increased suppressor T-cells, cytotoxic T-cells and Leu7+NK cells. The results indicate similar changes in the proportion of lymphocyte subsets and suggest immunologically activated and deficient conditions in both diseases. Immunomodulating effects of the treatment with low-dose prednisolone on some of the lymphocyte subsets in patients with these diseases were also supported by the study.     

Immunological studies of pulmonary infection with atypical mycobacteria. II. Depression of in vitro PPD-induced lymphocyte proliferation in patients with pulmonary atypical mycobacteriosis

To evaluate cell-mediated immune responses in patients infected with atypical mycobacteria (AM), mononuclear cells from patients were examined in vitro for purified protein derivatives (PPD) induced lymphocyte proliferation using combination of monoclonal antibodies and flowcytometry. Those from normal tuberculin-positive controls and chronic excreters with tuberculosis (chronics) were also examined. The results obtained were as follows: 1) In normal controls, PPD-S induced a significant proliferation of activated T cell subsets (Leu 4+ DR+, IL 2-R+ Leu 3+ and IL 2-R+ Leu 2+). A significant increase in pan T cells (Leu 4+), helper T cells (Leu 3+ 8-), suppressor T cells (Leu 2+ 15+) and B cells (Leu 4- DR+) was also observed. 2) In chronics, the pattern and degree of lymphocyte proliferation by PPD-S were similar to that observed in normal controls. 3) In AM, we found a significant proliferation of activated T cells (Leu 4+ DR+, IL 2-R+ Leu 3+, IL 2-R+ Leu 2+) and B cells (Leu 4- DR+) by PPD-S. However, the degree of lymphocyte proliferation in AM was clearly depressed as compared to normal controls and chronics. 4) In chronics, lymphocyte proliferation by PPD-S was significantly higher than that by PPD-B. In contrast, lymphocyte response by PPD-S was almost same as that by PPD-B in AM.     

Generation of CFUC suppressor T cells in vitro: VII. T derived colony inhibitory activity (Td/CIA) has no suppressor effect on in vitro immunoglobulin production

T derived colony inhibitory activity (Td/CIA) was obtained from unstimulated T cells from aplastic anemia patients (SAA), or from PWM primed normal T cells. Td/CIA suppressed CFUC growth of normal allogeneic marrow to less than 30% of expected growth. Td/CIA was then added to normal peripheral blood T and B cells, primed with PWM, to test whether it would interfere with in vitro immunoglobulin (Ig) production. When Td/CIA from normal T cells was added to cultures of T + B cells + PWM there was a 2-2.1-fold increase in Ig production. Similarly the addition of Td/CIA from SAA patients also resulted in a 1.4 up to 166-fold increase in Ig production. These results indicate that either (a) the targets for Td/CIA are expressed on hemopoietic but not on T and B cells, or (b) that Td/CIA inactivates an accessory cell which is essential for CFUC growth but not for the PWM driven in vitro B cell differentiation system.     

Analysis of natural killer cells in patients with aplastic anemia

We have analyzed natural killer (NK) cells in 43 patients with severe aplastic anemia, using cytotoxicity assays and microfluorometry with monoclonal antibodies, prior to and after treatment with antithymocyte globulin (ATG). Before treatment, natural killer cell activity (NKa) in both peripheral blood and bone marrow was markedly decreased in 76% of patients as compared with normal controls. Although we have measured low NKa in patients receiving large numbers of blood transfusions (means = 150 U of RBCs), six aplastic patients had low NKa in the absence of transfusions, and the average number of transfusions in the total population was low (means = 24). Purification of larger granular lymphocytes (LGLs) from peripheral blood of aplastic anemia patients failed to recover significant NKa. Most of these large granular lymphocytes showed few azurophilic granules. NKa was appropriately enhanced in these patients samples by exposure of mononuclear cells to either interleukin 2 (IL-2) or interferon (IFN). Analysis of peripheral blood phenotypic markers showed that cells bearing Leu 7 antigen were in the normal range in aplastic anemia (means = 12% +/- 2%; normal = 16% +/- 2%), but there was a deficiency of Leu 11+ cells (means = 8% +/- 2%; normal = 15% +/- 2%). The number of Leu 11+ cells was well correlated with NKa. In 13 of 22 patients treated with ATG, NKa returned to the normal range, and recovery of NKa was correlated to hematopoietic recovery. Our results suggest that deficient NKa is an intrinsic feature of aplastic anemia, and that the circulating cells in this disease are of the pre-NK cell stage.     

Expression of NK-lineage markers on peripheral blood lymphocytes with T- helper (Leu3+/T4+) phenotype in B cell chronic lymphocytic leukemia

Heterogeneity within lymphocyte subsets expressing T-helper (T4+/Leu3+) or T-suppressor (T8+/Leu2+) markers was analyzed in 38 patients with B cell chronic lymphocytic leukemia (B-CLL) and in 11 age-matched controls. Co-expression of NK-lineage markers (M1, Leu7) on Leu2+ or Leu3+ cells was investigated by two-color immunofluorescence, and the proportion of granular lymphocytes within each subset was determined by cytochemical staining for acid phosphatase. B-CLL patients and normal controls had similar absolute numbers of cells per microL with T- suppressor phenotype. However, the proportion of Leu2+ cells co- expressing the Leu7 antigen was higher in the B-CLL patients than in the control subjects (54 +/- 3% v 27 +/- 4%, P less than .0001). The absolute number per microL of cells with T-helper phenotype was somewhat decreased in B-CLL patients compared with normal subjects (649 +/- 104 v 799 +/- 33, P less than .02), with a consequent decrease of the helper/suppressor ratio. Furthermore, co-expression of the Leu7 and, more strikingly, of the M1 markers was increased significantly on Leu3+ cells from B-CLL patients compared with normal controls (11 +/- 2% v 2 +/- 0.7%, P less than .002 for Leu7 and 40 +/- 5% v 4 +/- 1%, P less than .00001 for M1). Cytochemical studies showed that a large proportion of Leu3+ cells from B-CLL patients were granular lymphocytes, as suggested by the co-expression of natural killer (NK) cell markers. The emergence of a population of Leu3+ granular lymphocytes with NK markers, which is barely detectable in normal subjects, may provide an explanation for the impairment of T cell functions repeatedly described in B-CLL.     

Effect of recombinant human granulocyte-macrophage colony-stimulating factor administration on the lymphocyte subsets of patients with refractory aplastic anemia

Human recombinant granulocyte-macrophage colony-stimulating factor (rhGM-CSF) was administered to 14 patients with refractory aplastic anemia (AA). The effect of rhGM-CSF therapy on the lymphocyte phenotype; on the proliferative responses to the mitogen phytohemagglutinin, Candida albicans, and tetanus toxoid antigens; and on the natural killer (NK) activity of the circulating lymphocytes was studied. Samples were collected before (baseline) and twice during the rhGM-CSF administration. The absolute number of circulating lymphocytes remained relatively constant during the first period, but experienced a significant increase (P less than .001) during the second period. The increase was most prominent in the B cells (P less than .001), but the T cells (P less than .016) also increased. Detailed investigation of lymphocyte subsets showed an increase of the markers CD38 (Leu17), HLA-DR, and the transferrin receptor throughout the treatment course giving evidence of lymphoid cell activation. The NK cell activity was suppressed (P less than .008) throughout the treatment. However, proliferative responses to phytohemagglutinin, Candida antigen, and tetanus toxoid were unaffected. Although the mechanism is not yet defined, GM-CSF does induce activation and increase in absolute lymphoid cell number, especially B cells, together with a decrease in NK cytotoxicity. The implication of these immune cell changes in relation to host resistance to microorganisms remains to be established.     

再生障碍性贫血患者细胞免疫功能与白细胞介素8水平检测

目的：探讨再生障碍性贫血（再障）的免疫发病机制,阐明Ｔ细胞亚群及ＩＬ－８ 在再障患者中的变化及临床意义。方法：用单抗试剂盒,采用ＳＡＰ法和双抗夹心酶联免疫吸附法（ＥＬＩＳＡ）对９ 例再障患者和１０ 例正常人外周血Ｔ 细胞亚群及血清ＩＬ－８ 含量进行测定。结果：再障患者外周血ＣＤ３、ＣＤ４ 亚群细胞减低,ＣＤ８ 亚群细胞增高,ＣＤ４／ＣＤ８ 降低,再障患者血清中ＩＬ－８ 含量明显高于正常对照组。结论：细胞免疫功能异常及造血负调控因子ＩＬ－８ 可能在再障发病中起一定的作用。     

Analysis of Natural Killer Cells in Patients with Idiopathic Autoimmune Hemolytic Anemia

A functional and phenotypic analysis of the circulating natural killer (NK) cell population was carried out in 9 patients with idiopathic autoimmune hemolytic anemia (IAHA). The NK-cell activity, assessed by a sensitive method based on the inhibition of target clone growth in plasma semisolid medium, was markedly decreased in all patients as compared with normal controls and was not restored by stimulation of the cells with recombinant alpha interferon (alpha-IFN). Analysis of peripheral blood phenotypic markers showed that cells bearing Leu7 and CD16 antigens numbered in the normal range. These findings suggest that IAHA patients exhibit a functional impairment of the NK compartment.     

Immunoarchitecture of the bone marrow in neutropenia: increased HNK-1 + cells define a subset of neutropenic patients

An immunoperoxidase technique was used to examine the distribution of lymphocyte subsets in bone marrow biopsies of 15 patients with neutropenia and seven non-neutropenic controls. The bone marrow of most patients and controls had similar distributions of immune effector cells characterized by a diffuse array of predominantly cytotoxic/suppressor T-cells and occasional nodular aggregates of helper T-cells. Cells displaying the natural killer cell marker HNK-1 were sparse in controls and most neutropenic patients. However, marked increases in marrow HNK-1 + cells were identified in four of the 15 patients. Three of these patients had diffuse HNK-1 + infiltrates associated with increased Leu 4+ (OKT-3+) T-cells while one had a nodular HNK-1+ infiltrate associated with small B-cell follicles. Each of these patients had clinical features similar to those described in the large granular lymphocyte (LGL) lymphocytosis (leukemia) syndrome, but only one of four demonstrated persistently increased numbers of LGLs in the peripheral blood. Thus, this study extends the association of neutropenia and increased numbers of cells with a T/NK phenotype to include patients whose bone marrow is the only demonstrable site of involvement. Since morphologic examination of the bone marrow could not identify the bone marrows with increased HNK-1+ cells, immunologic techniques are required to detect these cases.     

In vitro immunoglobulin production, proliferation, and cell markers before and after antithymocyte globulin therapy in patients with aplastic anemia

Peripheral blood lymphocytes from 16 aplastic anemia patients were studied for in vitro biosynthesis of immunoglobulins (Ig), proliferative responses, and cell markers before and after antithymocyte globulin (ATG) treatment in an attempt to identify immune functions that would be useful in predicting responses to ATG therapy. Six of the 16 aplastic anemia patients were complete responders to ATG therapy, two were partial responders, and eight failed to respond to ATG therapy. The proportion of E+, CD4, CD8, and surface Ig-positive cells did not correlate with in vitro lymphocyte functions nor clinical responses before or after ATG therapy. Lymphocyte proliferative responses to phytohemagglutinin, tetanus toxoid, alloantigens, or pokeweed mitogen were generally present before and after ATG therapy. When pokeweed mitogen, herpes simplex type I virus, and tetanus toxoid were used as probes to elicit in vitro Ig production using a hemolytic plaque assay, some patients had 1) B cells that failed to produce Ig, 2) T cells that failed to provide helper activity, and 3) T cells that exhibited excessive suppressor activity in the various antibody production systems. These measures of immune function, however, did not correlate with clinical responses to ATG therapy.     

Polarization of natural killer T cells towards an NKT2 subpopulation occurs after stimulation with alpha-galactosylceramide and rhG-CSF in aplastic anemia

Natural killer T (NKT) cells play an important role in the regulation of immune responses in a broad range of diseases, including autoimmune disorders, infectious diseases and cancer. So far, few studies have evaluated the roles of NKT cells in the pathogenesis of aplastic anemia (AA), an autoimmune disease. In this study, we investigated the quantitative and qualitative changes in NKT cells in bone marrow (BM) mononuclear cells of AA patients in response to in vitro stimulation with alpha-galactosylceramide. Compared to healthy controls, BM from AA patients had reduced fraction of NKT cells, which possessed a decreased potential to expand in vitro in response to alpha-galactosylceramide stimulation, producing more IFNgamma+ NKT1 cells. In the presence of rhG-CSF, the expansion capacity of NKT cells stimulated by alpha-galactosylceramide was significantly reduced in both AA and control groups, with the majority of the activated NKT cells expressing intracellular IL-4, and the fractions of IFNgamma+ NKT cells were significantly reduced. In summary, our results indicate that polarization of NKT cells towards the NKT2 subpopulation occurs after co-stimulation with alpha-galactosylceramide and rhG-CSF in AA.     

Antilymphocyte globulin therapy enhances impaired function of natural killer cells and lymphokine activated killer cells in aplastic anaemia

MHC-unrestricted cytotoxic lymphocytes, namely natural killer (NK) and lymphokine activated killer (LAK) cells, have been implicated in the regulation of haemopoiesis. To investigate the possible role of these lymphocytes in the pathogenesis of aplastic anaemia (AA), we studied their functions in the peripheral blood mononuclear cells (PBMC) and bone marrow mononuclear cells (BMMC) of patients with AA treated with antilymphocyte globulin (ALG). Before treatment, both NK and LAK activities in the PBMC of 25 patients were low (NK = 1.9 +/- 2.1 x 10(3) LU/l) LAK = 4.7 +/- 3.6 x 10(3) LU/l) compared to normal (NK = 6.0 +/- 3.0 x 10(3) LU/l, LAK = 10.0 +/- 3.5 x 10(3) LU/l) or multiply transfused (NK = 7.8 +/- 6.6 x 10(3) LU/l, LAK = 25.2 +/- 13.6 x 10(3) LU/l) controls. The NK and LAK activities in the BMMC in AA patients were not significantly different from those in PBMC. In all patients with low LAK and NK activities pre ALG there was an increase in activity 2-24 weeks after therapy which eventually reached normal levels and which was maintained for up to 2 years. Analysis of lymphocyte phenotypes in AA patients before treatment showed both significantly low mean proportion and absolute numbers of CD16+ cells compared to normals, which increased after therapy. Changes in MHC-unrestricted cytotoxicity and lymphocyte phenotypes post therapy were not correlated with haemopoietic recovery. These data suggest that ALG treatment can enhance the functions of MHC-unrestricted lymphocytes independently from haemopoiesis. It is unlikely that these cells play a role in the pathogenesis of AA.     

Natural killer cell activity in Sj?gren's syndrome and systemic lupus erythematosus: stimulation with interferons and interleukin-2 and correlation with immune complexes.

Natural killer (NK) cell activity and its stimulation by interferons (IFNs) and interleukin-2 (IL-2) are diminished in Sjögren''s syndrome and systemic lupus erythematosus (SLE). Serum samples of these patients often contain circulating immune complexes, which may influence NK cell activity. Sixteen patients with Sjögren''s syndrome (14/16 immune complex positive), 14 with SLE (9/14 immune complex positive), and 11 controls (immune complex negative) were studied. Mononuclear cells collected from a Percoll gradient were preincubated with recombinant IFN-alpha (rIFN-alpha) (100 U/ml), rIFN-gamma (1000 U/ml), rIL-2 (100 U/ml), or without cytokine. Natural killer cell activity was determined by incubating the mononuclear cells with carboxyfluorescein labelled K562 cells, and the percentage decrease of fluorescence was measured on an FACS Analyzer. In patients with Sjögren''s syndrome and SLE NK cell activity and the numbers of cells expressing the NK cell associated antigens CD16 and Leu7 were diminished compared with the controls. Interleukin-2 stimulated NK cell activity significantly in comparison with the non-stimulated value in all studied groups, whereas IFN-gamma only stimulated NK cell activity in both patient groups and IFN-alpha only in patients with Sjögren''s syndrome. There was no correlation between NK cell activity, with or without stimulation, and the immune complex concentrations. It is concluded that NK cell activity is decreased in Sjögren''s syndrome and SLE and that it may be partially restored by IL-2 and IFN-gamma in both diseases, and by IFN-alpha in Sjögren''s syndrome. The decrease of NK cell activity did not correlate with immune complex concentrations; on the other hand, decreased numbers of NK cells (CD16+ or Leu7+) and of cytokine concentrations might be important in the impaired NK cell activity in both diseases.     

B lymphocyte function in multiple myeloma: analysis of T cell- and monocyte-dependent antibody production

T-cell and B-cell functions were studied in 35 patients with untreated multiple myeloma (MM) and in 16 patients with MM treated with prednisolone, melphalan and vincristine. The numbers of CD4+ T cells were normal in untreated MM patients, but markedly decreased in treated patients, whereas CD8+ cell numbers were normal in untreated and treated patients. Mitogen-induced as well as antigen-induced lymphocyte proliferative responses were reduced, but not further affected by treatment. The antigen-induced proliferative responses by lymphocytes of treated, but not of untreated patients, correlated positively to the proportions of CD4+ cells among MNC. Taken together, the findings suggest selective loss of CD4+ subpopulations during cytotoxic treatment. Pokeweed mitogen (PWM)-induced Ig production was generally low, but significantly reduced Ig production was only seen in experiments employing MM B cells and monocytes co-cultured with irradiated T-enriched cells. Irradiated MM T cells displayed normal helper function when co-cultured with normal B cells stimulated with PWM. MM B cells and monocytes cultured with irradiated normal T cells produced little Ig; however, MM monocytes were not suppressive. In 2 of 3 patients with either IgG-kappa or IgA-kappa myeloma, the numbers of PWM-stimulated B cells that produced kappa chains were somewhat higher than those found among normal MNC. The impaired ability of antibody production by B cells from untreated MM patients seems to relate to intrinsic B cell defect(s) rather than to abnormal regulation by T cells or monocytes. However, disturbances in the functions of CD4+ cells may be observed in treated MM.     

Functional analysis of a clonal expansion of Leu 11 positive NK active lymphoid cells

A female patient with an unusual lymphoproliferative disease associated with marked neutropenia has been observed for 36 months. The expanded cell population consists of large lymphocytes, many of which contain large azurophilic granules with acid phosphatase activity. These cells were T3, T8, Tl1 and Leu 11 positive but lacked the Ml, T10, IL-2 receptor and HLA.DR antigens. The majority of these cells (60-70%) were also Leu 7 (HNK-1) positive. Strong natural killer (NK) activity was found in both the Leu 7 positive and negative cell populations. This cytotoxic activity was inhibited by monoclonal antibodies known to inhibit NK activity but was unaffected by antibodies which block T cell and T/NK cell cytotoxicity. Further functional analysis indicated that these cells suppressed normal T cell responses to mitogens, MLC responses and PWM induced B cell immunoglobulin synthesis. No effect on bone marrow progenitor cell growth was demonstrated. Antibody dependent cellular cytotoxic (ADCC) activity was barely detectable despite the presence of the Leu 11 antigen. Southern blot DNA analysis demonstrated clonal rearrangement of the T cell receptor β gene thereby confirming that this variant of T y lymphoproliferative disease was a neoplastic condition.     

Antigen-recognition sites of micromanipulated T cells in patients with acquired aplastic anemia

OBJECTIVE: Acquired aplastic anemia (AA) is a rare disorder characterized by pancytopenia and hypocellular bone marrow. Though experimental and clinical data suggest that AA represents a T cell-mediated disease, neither the immune response nor the nature of inciting antigen(s) have been characterized so far. The identification of a restricted T cell repertoire by PCR techniques in total lymphocyte populations supports an antigen-driven T cell response. In order to investigate the clonal composition, we analyzed the gene rearrangements of the T cell receptor (TCR) variable beta chain (Vbeta) at the single-cell level. PATIENTS AND METHODS: CD3(+) T lymphocytes were micromanipulated from peripheral blood and bone marrow samples of 8 AA patients and healthy controls. Subsequently amplified VDJ gene segments of the TCRVbeta chain were analyzed for functional rearrangements. More than 500 functionally rearranged TCR loci were studied for Vbeta/Jbeta gene segment usage and molecular composition of the complementary-determining region 3 (CDR3). RESULTS: In comparison to healthy controls, the Vbeta sequences confirmed a highly restricted T cell repertoire in AA patients at the single-cell level. Both in bone marrow and peripheral blood a predominance of Vbeta13 and Jbeta2S7 was observed. Furthermore, individual clonal T-cell expansion was identified in the majority of patients. However, deduced CDR3 amino acid sequences revealed a high variability without common motifs among the 8 patients. CONCLUSION: Individual clonal T-cell expansion with high diversity of the antigen-binding sites among the analyzed patients argues for the predominance of private inciting epitopes in AA.     

T helper cell defect related to severity in measles

Lymphocyte subpopulations, total T cells, T helper and T suppressor subpopulations as identified by monoclonal antibody and functional assays of suppressor cells using concanavalin A (Con A) were studied in 20 measles patients and compared to matched controls. Results were also related to severity of disease. Mononuclear cell (MNC) pokeweed mitogen (PWM) stimulation was also assessed. Severity of measles was assessed by lymphopenia, serum antibody and C3 levels and extent of pneumonia. T lymphopenia in patients was due to a decrease in OKT4+ cells and OKT8+ cells as compared to controls with the former being more severely affected. Patients with severe measles had a more profound reduction in both subsets (OKT4+ 356 +/- 65 cells/microliters mean +/- SEM; OKT8+ 466 +/- 41 cells/microliter) than those with mild disease (975 +/- 199 cells/microliters; 1,473 +/- 242 cells/microliters; p = 0.0432; 0.0038 respectively). Patients with severe depletion of OKT4+ cells had raised levels of C3 (an index of poor prognosis). Suppressor cell activity was unaffected by measles. MNC PWM stimulation was lower in patients than controls. No correlation was detected between numerical and functional assays of suppression although there was a significant correlation between PWM stimulation and OKT4+ cell numbers in the control group (p = 0.0407).     

Development and characterisation of T lymphocyte lines from human small intestinal biopsies.

T lymphocyte lines were developed from human small intestinal biopsies obtained at the time of gastroduodenoscopy. Lines were established as outgrowths from biopsy specimens in microculture using a combination of T cell mitogens, indomethacin, interleukin (IL-2) and autologous irradiated feeder cells. The predominant phenotype of T cells after six to 12 weeks in culture was CD2, CD3, and CD4 positive. Functionally, these T cell lines secreted IL-2 in response to stimulation with phytohemagglutinin (PHA) and phorbol 12-myristate 13-acetate (PMA) in combination, but not to PHA or PMA alone. Two to 7% of cells in each line expressed natural killer (NK) cell-associated markers--that is, Leu 7, CD16, and Leu 19. Moreover, such cells were cytotoxic for NK sensitive targets, but not for NK resistant targets or allogeneic or autologous Epstein Barr Virus (EBV) transformed B cells. Sufficient numbers of small intestinal lymphoid cells for study were previously available only from patients undergoing surgical resections of the small bowel. The ability to isolate and culture human small intestinal T lymphocytes from gastroscopic intestinal biopsies provides an important new tool for studies of human small intestinal lymphocytes.     

骨髓增生异常综合征和再生障碍性贫血患者T淋巴亚群及CD34阳性细胞的研究

目的：对骨髓增生异常综合征（MDS）和再生障碍性贫血（AA）患者的外周血T淋巴细胞亚群、NK细胞及骨髓CD34阳性细胞占单个核细胞（MNC）的比率进行测定,探讨两者细胞免疫异常及骨髓CD34阳性细胞与发病机制的关系。方法：用流式细胞术（FCM）对15例MDS患者,11例AA患者,12例正常对照组T淋巴细胞亚群、NK细胞及CD34阳性细胞占MNC的比率进行测定。结果：MDS患者外周血CD3＋T、CD4＋ T、CD8＋T淋巴细胞均较正常人组明显降低,CD4＋/CD8＋倒置。NK细胞CD16＋56也较正常人组低。AA患者CD4＋ T淋巴细胞稍低于正常人组,但CD8＋T淋巴细胞明显升高,表现为CD4＋/CD8＋也倒置。NK细胞正常。MDS患者CD34＋占骨髓MNC的比率明显高于正常组,AA患者骨髓MNC的比率低于正常组。结论：MDS和AA患者均存在免疫功能状态紊乱,二者的发病机制不同。CD34＋率的测定有助于二者的鉴别诊断,同时是判断MDS预后的简便、可靠的方法。