transforming-growth-factor-beta and Purpura--Thrombocytopenic--Idiopathic

Immune thrombocytopenia (ITP) is a common hematologic disorder characterized by isolated thrombocytopenia. In adults, ITP is more likely to be chronic, requiring individualised treatment and management. Corticosteroids and splenectomy are the most common therapy for ITP. However, these routine approaches failed in these patients with chronic ITP. The aim of this study was to evaluate the efficacy of immunomodulatory therapy with all-trans retinoid acid (ATRA) in adult patients with chronic ITP.. ATRA therapy was applied in a total of 35 patients with chronic ITP who failed with standard dose corticosteroids and/or splenectomy. The response ratio and the change of the T cell subsets including Th1, Th2, Th17 and Treg, were evaluated.. Complete response and overall response were observed in 10 (28.6%) and 19 patients (54.3%), respectively. Compared with the control group, a significant decreased level of Treg cells, IL-10 and Foxp3 expression were found in ITP patients. ATRA therapy could significantly increase the percentage of Treg cell, IL-10 level and Foxp3 expression.. Our findings indicate that ATRA therapy could induce significant changes of Treg cells to induce response in patients with chronic ITP.

Topics: Adult; Chronic Disease; Female; Humans; Immunologic Factors; Interleukin-10; Male; Middle Aged; Purpura, Thrombocytopenic, Idiopathic; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory; Transforming Growth Factor beta; Tretinoin

Immune thrombocytopenic purpura (ITP) is an autoimmune bleeding disorder characterized by production of auto-antibodies against platelet antigens. It is obvious that regulatory T cells (Tregs) have a major role in controlling immune homeostasis and preventing autoimmunity.To investigate the frequency and functions of Tregs, twenty ITP patients and twenty age- and sex-matched healthy controls were recruited. The peripheral blood mononuclear cells were isolated and the proportion of Tregs was defined by flow cytometry method. The expression of immune-regulatory markers, cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and glucocorticoid induced tumor necrosis factor receptor (GITR) were also assessed by quantitative Real-time PCR TaqMan method. For evaluation of Treg function, Tregs were enriched and their ability to inhibit proliferation of T cells was measured and levels of immune-regulatory cytokines IL-10 and TGF-β were also measured.Results showed that the frequency of Tregs and the mean fluorescence intensity of FOXP3 protein significantly decreased in ITP patients compared to those in healthy controls. In addition, there was a significant reduction in relative expression of both CTLA-4 and GITR mRNA in ITP patients (P=0.02 and P=0.006, respectively). The suppressive function of Tregs also diminished in ITP patients compared to that in controls. Both IL-10 and TGF-β cytokines were produced in lower amounts in ITP patients than controls.It could be concluded that alteration in Treg frequency and functional characteristics might be responsible for loss of self-tolerance and subsequently destructive immune responses observed in ITP patients.

Topics: Adolescent; Adult; CD4 Lymphocyte Count; Child; CTLA-4 Antigen; Female; Forkhead Transcription Factors; Gene Expression Regulation; Humans; Immune Tolerance; Interleukin-10; Male; Purpura, Thrombocytopenic, Idiopathic; T-Lymphocytes, Regulatory; Transforming Growth Factor beta

This study aims to investigate the changes of cytokines and the effect of programmed death ligand 1 (PD-L1) signaling pathway on T cell function in patients with immune thrombocytopenic purpura (ITP).Totally, 40 untreated ITP patients were recruited and 30 healthy people were recruited as the healthy control. Then whole blood of ITP patients and healthy control was collected, respectively. The sPD-L1/anti-PD-1 was used to activate or block the programmed death (PD-1)/PD-L1 signaling pathway. The expression of PD-1 and PD-L1 on peripheral blood mononuclear cells (PBMCs) were detected by flow cytometry. PBMCs were treated with cluster of differentiation (CD3), cluster of differentiation 28 (CD28), and phytohaemagglutinin (PHA) for 48 hours. Serum levels of sPD-1, sPD-L1, and cytokines were measured by enzyme-linked immunosorbent assay (ELISA).Compared with the healthy control group, the percentages of PD-1+CD3+CD4+ T cells and PD-L1+HLA-DR+CD11c+ DC cells were increased in ITP patients. The levels of interferon-gamma (IFN-γ), interleukin-17 (IL-17), and sPD-1 in the serum of ITP patients were increased, while IL-4 and transforming growth factor-β (TGF-β) were decreased. Additionally, the level of sPD-1 was negatively correlated with the platelet count. Consistently, after treatment with CD3, CD28, and PHA, IFN-γ and IL-17 levels in culture supernatant of PBMCs from ITP patients were significantly higher than those from healthy controls whereas IL-4 and TGF-β levels were significantly lower. Furthermore, IFN-γ and IL-17 levels secreted by PBMCs from ITP patients decreased after sPD-L1 administration, however, IL-4 and TGF-β levels were increased. The level of IFN-γ in ITP group remained higher after anti-PD-1 blockage, but the levels of IL-4, TGF-β, and IL-17 were not significantly influenced.sPD-1 may cause the dysfunction of PD-1/PD-L1 signaling pathway, and its level is related to the severity of ITP patients. Activation of PD-1/PD-L1 with sPD-L1 may restore the imbalance of Th1/Th2 and Treg/Th17 cell subtypes in ITP patients but anti-PD-1 may exacerbate disease by enhancing IFN-γ production.

Topics: Adult; B7-H1 Antigen; Case-Control Studies; CD28 Antigens; CD3 Complex; Cytokines; Female; Humans; Interferon-gamma; Leukocytes, Mononuclear; Male; Middle Aged; Phytohemagglutinins; Programmed Cell Death 1 Receptor; Purpura, Thrombocytopenic, Idiopathic; Signal Transduction; T-Lymphocytes; T-Lymphocytes, Regulatory; Th1-Th2 Balance; Th17 Cells; Transforming Growth Factor beta

To detect the levels of Treg, Th17, Th9 cells and expression of transforming growth factor-β (TGF-β), interleukin-17 (IL-17) and interleukin-9 (IL-9) in peripheral blood of patients with immune thrombocytopenia (ITP) and to explore its role in the pathogenesis of ITP.. Fifty-four patients with ITP (ITP group) and 40 healthy volunteers (control group) were selected in our hospital. The of Treg, Th17 and Th9 cells in peripheral blood of 2 groups were measured by flow cytometry, and the expression of cytokines, such as TGF-β, IL-17 and IL-9 in the peripheral blood of 2 groups were detected by enzyme linked immunosorbent assay (ELISA).. The level of Treg cells in the peripheral blood of the ITP group was significantly decreased in comparison with the control group, while the levels of Th17 and Th9 cells significantly increased in comparison with the control group (all P<0.01). The expression of cytokine such as TGF-β in the peripheral blood of the case group significantly decreased in comparison with the control group, while the expression levels of IL-17 and IL-9 significantly increased in comparison with the control group (P<0.01). The results of Pearson correlation analysis showed that there was a positive correlation between the level of Treg cells and platelet count (PLT) in peripheral blood of the ITP group (r=0.35, P<0.05), and there were negative correlation between the level rate of Th17, Th9 cells and Plt count (r=-0.37, -0.43, P<0.05); there was a positive correlation between the expression of the TGF-β in the ITP group and Plt count (r=0.46, P<0.05), while the expression of IL-17 and IL-9 showed negative correlation with PLT (r=-0.48, -0.54, P<0.05).. The percentage of Treg, Th17 and Th9 cells in the peripheral blood of patients with ITP is abnormal, and the expression of TGF-β, IL-17 and IL-9 also is abnormal, which may play an important role in the pathogenesis of ITP.

Topics: Flow Cytometry; Humans; Interleukin-17; Interleukin-9; Purpura, Thrombocytopenic, Idiopathic; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory; Transforming Growth Factor beta

To explore the role of Treg cells in the pathogenesis of idiopathic thrombocytopenic purpura (ITP).. The ITP mouse model was established, the Treg cell ratio in peripheral blood and spleen was detected by flow cytometry, the CD4+ CD25+ T cells were sorted by immunomagnetic beads, the Treg cell associated transcription factors (Foxp3, Smad7, STAT5 and Akt-1) and cytokines (IL-10, TGF-β) in CD4+ CD25+ T cells were enriched from spleen mononuclear cells, and the mRNA expression of Treg cell was measured by real-time PCR.. The ratio of Tregs in peripheral blood and spleen decreased significantly in ITP mouse, as compared with the controls (P<0.01). In addition, the mRNA expression of IL-10, TGF-β and Foxp3 decreased significantly in spleen CD4+ CD25+ T cells (P<0.05). Expression of Smad 7 mRNA was higher than that of controls.. The alteration in Treg frequency and function may be responsible for the immune dysfunction in ITP disease. It is also speculated that the lower mRNA expression of Foxp3 and higher mRNA expression of Smad 7 may inhibit the proliferation and differentiation of Treg cells.

Topics: Animals; Flow Cytometry; Forkhead Transcription Factors; Interleukin-10; Mice; Purpura, Thrombocytopenic, Idiopathic; Real-Time Polymerase Chain Reaction; RNA, Messenger; Smad7 Protein; Spleen; T-Lymphocytes, Regulatory; Transforming Growth Factor beta

To detect the expression levels of CD4(+) CD25(+) CDl27(low) Treg cells, TGF-β and Notch1 mRNA in peripheral blood of the patients with idiopathic thrombocytopenic purpura (IPT) before and after treatment, and to investigate their significance in the pathogenesis of ITP.. Peripheral blood was collected from 30 newly diagnosed patients with ITP and 20 normal controls, then the number of CD4(+) CD25(+) Treg and CD4(+) CD25(+) CDl27(low) Treg were detected by the flow cytometry. Plasma TGF-β level was determined by ELISA. Total RNA was extracted and the expression level of Notch1 mRNA was measured by real-time Q-PCR.. The expression levels of CD4(+) CD25(+) CDl27(low) Treg and CD4(+) CD25(+) Treg in newly diagnosed ITP group were significantly lower than those in normal controls. After treatment, the proportion of Tregs increased to (5.17% ± 0.74%) and (4.16% ± 0.68%), and was higher than that in newly diagnosed patients. The TGF-β level in peripheral blood of newly-diagnosed patients was obviously lower than that in normal controls, and was (961.53 ± 60.10) ng/L after treatment and was significantly higher than that in newly diagnosed patients; the expression level of Notch1 mRNA in peripheral blood of patients in newly-diagnosed group was obviously lower than that in control, and was (1.35 ± 0.10) after treatment that was higher than that in newly-diagnosed group. After treatment, the proportion of Treg cells, level of TGF-β and erpression level of Notch1 mRNA in effective group were higher than those in effective group, improved group and ineffective group, and there was significant difference (P <0.01). The expression level of TGF-β and Notch1 mRNA in ITP patients possitively correlated to CD4(+) CD25(+) CDl27(low) (P <0.01).. The levels of CD4(+) CD25(+) CDl27(low) Treg, TGF-βand Notch1 mRNA in peripheral blood of the patients with ITP are significantly lower than those of normal control, suggesting that there is significant abnormal immunoregulation in ITP patients. In the ITP patients the levels of CD4(+) CD25(+) CDl27(low) Treg postively correlated with Notch1 mRNA expression, indicating that Notch signal may be revalent to Treg's immunosuppression function.

Topics: Enzyme-Linked Immunosorbent Assay; Flow Cytometry; Humans; Purpura, Thrombocytopenic, Idiopathic; Real-Time Polymerase Chain Reaction; Receptor, Notch1; RNA; RNA, Messenger; T-Lymphocytes, Regulatory; Transforming Growth Factor beta

IL-35 is a novel heterodimeric anti-inflammatory cytokine consisting of Epstein-Barr virus-induced gene 3 (EBI3) and the p35 subunit of IL-12. IL-35 has been shown to possess the potency of inhibiting the CD4+ effector T cells and alleviating autoimmune diseases. In the study we investigated the levels of IL-35 as well as its prospective role in immune thrombocytopenia (ITP).ELISA was adopted to measure plasma IL-35, TGF-β and IL-10 levels. The mRNA expression levels of P35 and EBI3 in peripheral blood mononuclear cells (PBMCs) were studied based on real-time quantitative PCR. The correlation between plasma cytokine levels and clinical parameters was analyzed. Significantly lower plasma IL-35 levels were found in active ITP patients compared with those in remission (p = 0.017) and the healthy controls (p < 0.001). In active ITP patients, the plasma IL-35 levels displayed a significantly positive correlation with platelet counts (r = 0.5335, p < 0.0008). Further, P35 mRNA expression levels were lower in patients with active ITP than patients in remission (p = 0.033) and normal controls (p = 0.016).Thus, for the first time, this research reported a dramatically decreased IL-35 levels in ITP patients, suggesting that IL-35 may be involved in the pathogenesis of ITP.

Topics: Adolescent; Adult; Aged; Case-Control Studies; Female; Gene Expression; Humans; Interleukin-10; Interleukin-12 Subunit p35; Interleukins; Leukocytes, Mononuclear; Male; Minor Histocompatibility Antigens; Platelet Count; Purpura, Thrombocytopenic, Idiopathic; Remission Induction; RNA, Messenger; Transforming Growth Factor beta

Immune thrombocytopenia (ITP) is an autoimmune disorder caused by IgG anti-platelet autoantibodies. Thrombopoietin (TPO) receptor agonists are highly effective in inducing the recovery of platelet counts in ITP patients. Although these agents are thought to promote platelet production without affecting the autoimmune pathogenesis of the disease, a small subset of ITP patients exhibits sustained platelet recovery after treatment termination. To investigate mechanisms involved in this sustained recovery, we evaluated the effects of short-term TPO treatment using a mouse ITP model generated by Foxp3(+) T regulatory cell (Treg) depletion. After treatment, platelet recovery was sustained, along with complete suppression of both anti-platelet autoantibody production and T-cell responses to platelet autoantigens. TPO treatment also promoted the peripheral induction of Foxp3(+) Tregs in conjunction with elevated circulating TGF-β levels. In summary, thrombopoietic agents are capable of inducing immune tolerance to platelet autoantigens, thereby suppressing the autoimmune pathogenesis of ITP.

Topics: Animals; Autoantibodies; Blood Platelets; Disease Models, Animal; Immune Tolerance; Isoantigens; Mice; Purpura, Thrombocytopenic, Idiopathic; T-Lymphocytes, Regulatory; Thrombopoietin; Transforming Growth Factor beta

This study was aimed to investigate the T cell (helper T cells) immune status in ITP patients and its relation with therapeutic response. 20 de novo ITP patients were enrolled (8 males, 12 females) with a median age of 41 (20 to 81). Real-time RT-PCR method was used to measure the gene expression of Th cells including T-bet, IFN-γ, GATA-3, TGF-β, Foxp3, IL-2, IL-4 in PBMNC of ITP patients before and after conventional dose of prednisone therapy [1 mg/(kg·d)] and in PBMNC of 20 normal controls. The results showed that T-bet, IFN-γ and IL-2 were significantly over-expressed in PBMNC of ITP patients before treatment compared with that in normal controls (p < 0.01), and compared with that before treatment, T-bet, IFN-γ, and IL-2 were markedly down-regulated in ITP patients after treatment. Before treatment, the expressions of Foxp3, TGF-β, GATA3 and IL-4 in ITP patients did not show difference from normal controls, while after treatment Foxp3 were more up-regulated than that before treatment (p < 0.05). After treatment, TGF-β expression showed a different pattern between old and young patients. TGF-β expression was down-regulated (p < 0.05) among ITP patients younger than 60, while up-regulated in older patients. It is concluded that there is an imbalance of Th1/Th2/Treg cytokines in ITP patients, which can be reversed by glucocorticoid treatment. The conventional dose of glucocorticoid may be regarded as effective therapy for de novo ITP patients, it may correlate with improvement of imbalance between Th1/The2/Treg cytokines.

Topics: Adult; Aged; Aged, 80 and over; Case-Control Studies; Female; Forkhead Transcription Factors; Gene Expression; Gene Expression Regulation; Glucocorticoids; Humans; Interferon-gamma; Interleukin-2; Male; Middle Aged; Purpura, Thrombocytopenic, Idiopathic; T-Box Domain Proteins; T-Lymphocytes, Helper-Inducer; Transforming Growth Factor beta; Young Adult

The data on polarization of the immune system towards T helper 1 (Th1) or T helper 2 (Th2) cells in immune thrombocytopenic purpura (ITP) are limited and contradictory. Th17 characterized by the production of Interleukin 17 (IL-17) has been shown to play a crucial part in the induction of autoimmune diseases. To further investigate the role of Th cytokines in the pathogenesis of ITP, we measured the plasma concentration of three Th17-associated cytokines [IL-17, transforming growth factor-ss (TGF-ss), IL-6] and Th1 cytokine interferon-gamma (IFN-gamma) in ITP patients, and evaluated their clinical relevance. The concentration of IL-17, TGF-ss, IL-6, and IFN-gamma in plasma specimens from 29 adults with chronic ITP and 38 controls was analyzed by enzyme-linked immunosorbent assay method. No significant differences of Th17 cytokines (IL-17, TGF-ss, and IL-6) and Th1 cytokine (IFN-gamma) concentration were observed between patients with active ITP and the control group. And the IFN-gamma/IL-17 ratio representing Th1/Th17 cytokine profile was not significantly different between ITP patients and control, either. However, significantly positive correlation between IL-6 and IFN-gamma in ITP patients was observed (r = 0.48, P = 0.01). Among the ITP patients, Plasma IL-17 levels in male were marginally higher than those in female, while similar for TGF-ss, IL-6 or IFN-gamma. There was a significantly positive correlation between age and IL-6 concentration in ITP patients (r = 0.56, P = 0.0002), while no statistical significance between age and the other three cytokines. No significant correlation between cytokine concentrations and platelets or megakaryocytes number was found in ITP patients. In summary, ITP may not be associated with changes of plasma Th17 and Th1 cytokine concentrations relative to control population.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Case-Control Studies; Female; Humans; Interferon-gamma; Interleukin-17; Interleukin-6; Male; Middle Aged; Purpura, Thrombocytopenic, Idiopathic; T-Lymphocyte Subsets; T-Lymphocytes, Helper-Inducer; Transforming Growth Factor beta

To investigate whether transforming growth factor-beta 1 (TGF-beta 1) gene polymorphisms have a role in the development, clinical progress, and treatment response in children with idiopathic thrombocytopenic purpura (ITP).. Thirty-five children with acute ITP, 40 children with chronic ITP, and 97 healthy children were enrolled. After genomic DNA was extracted, TGF-beta 1 gene 509 (C-->T), codon 25 (Arg-->Pro), and codon 10 (Leu-->Pro) polymorphisms were studied using a coupled polymerase chain reaction-restriction enzyme digestion method.. The genotype and allele frequencies of TGF-beta 1 polymorphisms between acute ITP, chronic ITP, and control group did not differ significantly. No significant association was found between TGF-beta 1 polymorphisms and therapy response.. These results demonstrate that the frequency of TGF-beta1 gene 509 (C-->T), codon 25 (Arg-->Pro), and codon 10 (Leu-->Pro) polymorphisms and alleles do not play a role as a genetic risk factor in the development and clinical progress of ITP. Different results may be obtained with further studies involving larger patient populations and other TGF-beta 1 gene polymorphisms.

Topics: Adolescent; Child; Child, Preschool; Codon; Female; Genetic Predisposition to Disease; Humans; Infant; Male; Polymorphism, Genetic; Purpura, Thrombocytopenic, Idiopathic; Risk Factors; Transforming Growth Factor beta; Transforming Growth Factor beta1

Chronic idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder in which activated T-helper (Th) cells and different Th-cell cytokines might play an important role. We have recently reported that chronic ITP patients in remission had elevated plasma levels of the Th3 cytokine transforming growth factor-beta1 (TGF-beta1), possibly as a part of a bystander immune suppression. In the present study we found that, in ITP patients with active disease [platelet count (plc) < 50 x 10(9)/l], mitogen-stimulated peripheral blood mononuclear cells (PBMC) had a significantly reduced production of TGF-beta1 (444 +/- 178 pg/ml; n = 6) compared with patients with plc 50-150 x 10(9)/l (1293 +/- 374 pg/ml; n = 9; P < 0.05), patients with plc >150 x 10(9)/l (1894 +/- 244 pg/ml; n =12; P <0.005) and healthy controls (1698 +/- 241 pg/ml; n = 10; P < 0.01). Nineteen per cent of ITP patients expressed a platelet-induced PBMC proliferation. Surprisingly, 22% of the ITP patients had a PBMC proliferation below the normal range, i.e. a suppressed proliferation in the presence of platelets; five of these six patients had active disease. In summary, this study demonstrated that chronic ITP patients with active disease had reduced PBMC production of the Th3 cytokine TGF-beta1. This result gives further support to the theory that chronic ITP in active phase is associated with a downregulated Th3-response.

Topics: Acute Disease; Biological Assay; Blood Platelets; Case-Control Studies; Cell Division; Cells, Cultured; Leukocytes, Mononuclear; Mitogens; Purpura, Thrombocytopenic, Idiopathic; Transforming Growth Factor beta

Bystander immune suppression has been demonstrated in experimental models of oral immune tolerance induction. This phenomenon is associated with expression of transforming growth factor (TGF)-beta1 and T-helper cell (Th) 2 cytokines. We have studied serum levels of Th cytokines and B- and T-lymphocyte subsets in chronic idiopathic thrombocytopenic purpura (ITP), a disorder in which the production of platelet autoantibodies might be caused by a cytokine network dysregulation. Forty-six patients with ITP were separated into three groups depending on the platelet count (pltc): (1) < 50 x 10(9)/l, (2) 50-150 x 10(9)/l and (3) > 150 x 10(9)/l. We found significantly elevated plasma levels of the Th3 cytokine TGF-beta1 in patients with pltc >150x10(9)/l (23.5+/-2.8ng/ml), compared with patients with pltc <50x10(9)/l (2.3+/-0.6 ng/ml; P<0.0001), patients with pltc 50-150x 10(9)/l (7.2+/-1.7 ng/ml; P<0.0001) and healthy volunteers (9.8+/-1.3 ng/ml; P<0.01). The serum levels of the Thl cytokines interleukin (IL)-2 and interferon (IFN)-y were below the detection limits of the assays. Likewise, the Th2 cytokine IL-4 was not detectable or was very low both in patients and controls. The serum levels of IL-10, a Th2 cytokine, were within the assay range and patients with pltc <50 x 10(9)/l had significantly lower levels (0.6+/-0.1 pg/ml) than both patients with pltc 50-150 x 10(9)/l (1.8 +/- 0.1 pg/ml; P<0.005) and healthy volunteers (1.4+/-0.1 pg/ml; P<0.005). Furthermore, patients with pltc <50 x 10(9)/l and splenectomised patients had significantly higher levels of CD4 + CD25 + activated T cells [26.2 +/- 14.8% (P<0.05) and 26.7+/-11.9% (P<0.005), respectively] than healthy controls (16.5+/-4.0%). Also, the number of natural killer (NK) cells among patients with pltc >150 x 10(9)/l were significantly elevated (26.6+/-16.0%; P<0.05) compared with controls (17.4+/-7.6%). In conclusion, our data corroborate previous findings of elevated numbers of activated T cells in chronic ITP patients with active disease, but neither a clear-cut Th1 nor a Th2 serum cytokine profile could be established. However, ITP in remission was associated with elevated TGF-beta1, which might be a part of a bystander immune suppression. We propose that the effect of possible expression of TGF-beta1 by oral immune tolerance induction deserves to be explored in ITP patients with an active disease.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Chronic Disease; Cytokines; Female; Humans; Immune Tolerance; Interferon-gamma; Interleukin-1; Interleukin-4; Lymphocyte Activation; Lymphocyte Subsets; Male; Middle Aged; Purpura, Thrombocytopenic, Idiopathic; Remission Induction; Th1 Cells; Th2 Cells; Transforming Growth Factor beta; Transforming Growth Factor beta1

A case of Evans' syndrome with IgM deficiency and lymphopenia was studied before and after splenectomy. The lymphopenia was as a result of profound reduction of CD4 and CD8 cells. Study of cytokine secretion before splenectomy revealed a spontaneous Th1- and Th2-type cytokine production, and complete suppression of transforming growth factor (TGF)-beta. After splenectomy, the patient achieved clinical remission, the natural killer (NK) cell number increased and the pattern of cytokine production showed normalization of interleukin (IL)-2, IL-4, IL-10, TGF-beta and abolition of interferon (IFN)-gamma production. We conclude that splenectomy had a beneficial effect owing to an increase in NK cells and an associated increase in TGF-beta production.

Topics: Anemia, Hemolytic, Autoimmune; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Child; Cytokines; Humans; Immunoglobulin M; Interferon-gamma; Interleukin-10; Interleukin-2; Interleukin-4; Killer Cells, Natural; Lymphocyte Count; Lymphopenia; Male; Purpura, Thrombocytopenic, Idiopathic; Splenectomy; Syndrome; Th1 Cells; Th2 Cells; Transforming Growth Factor beta