Humans ; Liver Diseases ; diagnosis ; pathology ; Prognosis ; T-Lymphocytes, Regulatory

Aplastic anemia (AA) is an autoimmune disease characterized by destruction of hematopoietic tissue resulting in hyperfunction of effector T-lymphocytes. Recent studies indicate that Th17 and Treg cells are functionally antagonistic each other, and the increase of Th17 cells and decrease of Treg cells are closely related with AA. In vivo experiments showed that both anti-IL-17 treatment and Treg cell infusion can protect against immune-mediated bone marrow failure in mouse with AA. This review summarizes the recent progress of study on imbalance of Th17/Treg cells in AA, so as to explore the pathogenesis of AA and provide approach to clinical treatment. The main problems that are discussed in this review include biological characteristics of Th17/Treg cells, the regulation of Th17/Treg cell balance and related cytokines, the relationship between Th17/Treg cells and AA.
Anemia, Aplastic ; immunology ; pathology ; Humans ; T-Lymphocytes, Regulatory ; immunology ; Th17 Cells ; immunology

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal disorder of hematopoiesis due to the inactivation of PIG-A gene. However, the presence of mutant PIG-A gene in a group of hematopoietic cells is not enough for the development of PNH, immunologic injury and apoptotic effects are considered to play an important role in clonal expansion. Knowledge of the molecular mechanisms leading to PNH has substantially increased in the past decades, which remarkably advances the diagnostic modalities and treatment approaches of patients with PNH. Though great progress has been made because of targeted therapy method, the challenges are still ahead. In this review the advances of studies on mechanism, laboratorial diagnosis and therapeutic protocols of PNH are summarized.
Complement System Proteins ; Hemoglobinuria, Paroxysmal ; diagnosis ; genetics ; pathology ; therapy ; Humans ; Membrane Proteins ; genetics ; T-Lymphocytes, Regulatory

T cell immunity and phagocytic activity were studied in the blood of patients with IgA nephropathy in order to clarify their roles in the pathogenesis of IgA nephropathy. The percentages of total T lymphocytes, helper T cell and suppressor T cells were significantly reduced in patients. A significantly elevated helper T cell/suppressor T cell ratio in patients showed a predominant reduction in suppressor T cells. There was a significant relationship between histologic findings and helper T cell/suppressor T cell ratio in patients. Natural Killer (NK) cell activity was significantly reduced but the lymphocyte response after phytohemagglutinin (PHA) stimulation was not in patients. ConA-induced suppressor cell activity was not depressed despite of a decrease in suppressor T cells in patients. Phagocytic activity of polymorphonuclear leucocytes (PMNs) ingesting yeasts was significantly reduced in patients. Also an inverse correlation was found between serum IgA levels and phagocytic activity of PMN. It is concluded that suppressor T cell defects, depressed phagocytic activity and impaired NK cell activity may play a role in the pathogenesis of IgA nephropathy.
B-Lymphocytes/immunology ; Glomerulonephritis, IGA/*immunology/pathology ; Humans ; Killer Cells, Natural/immunology ; Neutrophils/immunology ; *Phagocytosis ; T-Lymphocytes/*immunology ; T-Lymphocytes, Regulatory/immunology

Both T helper IL-17-producing cells (Th17 cells) and regulatory T cells (Tregs) have been found to be increased in malignant pleural effusion (MPE). However, the possible imbalance between Th17 cells and Tregs, as well as the association of Th17/Treg and Th1/Th2 cells in MPE remains to be elucidated. The objective of the present study was to investigate the distribution of Th17 cells in relation to Tregs, as well as Th1/Th2 balance in MPE. The number of Th17, Tregs, Th1, and Th2 cells in MPE and peripheral blood was determined by using flow cytometry. The relationship among the number of Th17, Tregs, Th1, and Th2 cells was explored. It was found that the number of Th17, Tregs, Th1, and Th2 cells was all increased in MPE as compared with the corresponding peripheral blood. The number of Th17 cells was correlated negatively with Tregs in MPE, but not in blood. Th17 cells and Th17/Treg ratio were positively, and Tregs were negatively, correlated with Th1 cells, but not with either Th2 cells or Th1/Th2 ratio in MPE. This study supports earlier data that both Th17 cells and Treg are present at higher frequencies in MPE than in the autologous blood. For the first time, we show that Th17/Treg imbalance exists in MPE.
Adult ; Female ; Humans ; Male ; Middle Aged ; Pleural Effusion, Malignant ; immunology ; pathology ; T-Lymphocytes, Regulatory ; immunology ; pathology ; Th17 Cells ; immunology ; pathology

The multiple myeloma (MM), the second most common hematologic malignancy, is malignant proliferative disease of plasma cells. Although the application of many targeted drugs has significantly prolonged the survival time of MM patients, it is still an incurable disease. In recent years, the immunosuppression caused by interaction between tumor microenvironment(TME) and tumor cells has attracted people's attention gradually. As a kind of immunosuppressive cells in TME, regulatory T cells (Treg) play an important role in the progress of MM. Treg is related to the proliferation and metastasis of tumors, and can lead to the progress of MM by promoting the angiogenesis and generating immunosuppressive TME. In this review, we briefly summarized the latest research progress on the impact of Treg on the pathogenesis of MM.
Humans ; Multiple Myeloma/pathology* ; T-Lymphocytes, Regulatory/pathology* ; Immune Tolerance ; Plasma Cells/pathology* ; Immunosuppression Therapy ; Tumor Microenvironment

Adult ; Biopsy ; Fatty Liver ; complications ; immunology ; pathology ; Female ; Hepatitis B, Chronic ; complications ; immunology ; pathology ; Humans ; Male ; T-Lymphocytes, Regulatory ; immunology

Adult ; Female ; Humans ; Liver ; immunology ; pathology ; Liver Cirrhosis, Biliary ; immunology ; pathology ; Male ; Middle Aged ; T-Lymphocytes, Regulatory ; immunology

OBJECTIVETo investigate liver fibrosis-related changes of CD4⁺CD25⁺Foxp3+ regulatory T cells (Tregs) in peripheral blood and in liver-infiltrating lymphocytes (LILs) using a mouse model.

METHODSC57BL/6 mice were randomly divided into a model group and a control group. The model group received intraperitoneal injection of carbon tetrachloride (CC1₄) to induce liver fibrosis, and the control group received an equal volume of physiological saline. Serum was collected for detection of alanine aminotransferase level. Histopathological changes in liver were assessed by microscopic observation of tissues stained by hematoxylineosin and Masson. Frequencies of peripheral and intrahepatic Tregs, NK1.1⁺ cells, CD4⁺ and CD8⁺ cells were analyzed by flow cytometry. Intrahepatic Foxp3+ cells were detected by immunofluorescence. Liver expression of IL-6, IL-10, TGFb and Foxp3 was measured by RT-PCR detection of mRNA .Inter-group differences were evaluated by t-test.

RESULTSThe model group showed a significantly higher frequency of intrahepatic CD25⁺Foxp3⁺/CD4⁺ Tregs (10.63% ± 1.50% vs. control group:1.80% ± 0.66%; P less than 0.01) but only slightly higher frequency of peripheral Tregs (6.00% ± 0.62% vs. 5.33% ± 2.86%). The model group also showed significantly higher levels of intrahepatic Foxp3+ cells and of Foxp3 mRNA (both P less than 0.05), but significantly lower frequencies of NK1.1 cells in LILs (9.53% ± 2.25% vs. 19.80% ± 5.97%; P less than 0.05) and in peripheral blood (0.38% ± 0.13% vs. 1.06% ± 0.63%; P less than 0.05). The CD4⁺ cell frequency and the CD4⁺/CD8⁺ ratio were lower in LILs and peripheral blood of the model group, but none differed significantly from the control group. The intrahepatic expression of TGFb mRNA was significantly higher in the model group (P less than 0.01).

CONCLUSIONIn liver fibrosis, intrahepatic CD4⁺CD25⁺Foxp3+ Tregs are increased while NK1.1+ cells are decreased. Tregs may suppress NK1.1+ cells through a mechanism involving TGFb.

Animals ; Liver ; metabolism ; pathology ; Liver Cirrhosis, Experimental ; blood ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred C57BL ; T-Lymphocytes, Regulatory

Animals ; CD4-Positive T-Lymphocytes ; immunology ; Humans ; Periodontal Diseases ; immunology ; pathology ; T-Lymphocytes, Regulatory ; immunology ; Th1 Cells ; immunology ; Th17 Cells ; immunology ; Th2 Cells ; immunology