Understanding germinal center reactions is crucial not only for the design of effective vaccines against infectious agents and malignant cells but also for the development of therapeutic intervention for the treatment of antibody-mediated immune disorders. Recent advances in this field have revealed specialized subsets of T cells necessary for the control of B cell responses in the follicle. These cells include follicular regulatory T cells and Qa-1-restricted cluster of differentiation (CD)8+ regulatory T cells. In this review, we discuss the current knowledge related to the role of regulatory T cells in the B cell follicle.
Germinal Center ; Immune System Diseases ; T-Lymphocytes ; T-Lymphocytes, Helper-Inducer ; T-Lymphocytes, Regulatory* ; Vaccines

OBJECTIVE: To explore the role of follicular helper T cell (Tfh)/ follicular regulatory T cell (Tfr) imbalance in B-cell lymphoma (BCL). METHODS: Sixteen BCL patients who were admitted to the Department of Hematology of The First People's Hospital of Yichang and 20 healthy people from December 2019 to November 2020 were enrolled and respectively divided into observation group and control group. The levels of Tfh and Tfr in peripheral blood were detected by flow cytometry. The changes of Tfh, Tfr, and Tfh/Tfr ratio were compared and the relationship between Tfh/Tfr ratio and efficacy, prognosis was analyzed. RESULTS: Compared with the healthy controls, Tfh and Tfh/Tfr ratio in peripheral blood of the BCL patients increased (P<0.05, P<0.01), while levels of Tfr was decreased (P<0.01). After chemotherapy, Tfh and Tfh/Tfr ratio in peripheral blood of the BCL patients decreased significantly than before chemotherapy (P<0.01), but Tfr was no significant difference. Multivariate analysis showed that Tfh and Tfh/Tfr ratio were positively correlated with international prognostic index (IPI) score and Ann Arbor stage (r=0.626, 0.564, 0.573, 0.608, respectively), while Tfr negatively (r=－0.504, －0.542, respectively). According to the average value of Tfh/Tfr ratio at initial diagnosis, BCL patients were divided into Tfh/Tfr high ratio group and low ratio group. It was found that the complete remission (CR) rate, overall response rate (ORR), and survival time in the high ratio group were significantly lower than the low ratio group (P<0.01). CONCLUSION There is an imbalance of Tfh/Tfr ratio in peripheral blood of the BCL patients, and those with a high Tfh/Tfr ratio have lower CR, ORR and shorter survival time.
Flow Cytometry ; Humans ; Lymphoma, B-Cell ; T Follicular Helper Cells ; T-Lymphocytes, Helper-Inducer ; T-Lymphocytes, Regulatory

To investigate the effects of chemerin on helper T cells 9 (Th9)/regulatory T cells (Treg) in patients with psoriasis and the potential molecular mechanisms.
 Methods: Twenty-five patients with psoriasis and twenty healthy volunteers were selected for this study. CD4+ T cells were isolated from peripheral blood of samples by magnetic bead separation. The levels of chemerin and its receptor chemR23 were detected by real-time RT-PCR and ELISA. CD4+ T cells isolated from the healthy volunteers were treated with different concentrations of chemerin (50, 100, 150, 200 ng/mL), then cell viability was detected by MTT assay. The expression of inflammatory molecules and Th9/Treg were detected by ELISA and flow cytometry, respectively.
 Results: The expressions of chemerin and chemR23 in peripheral blood from patients with psoriasis were higher than those in healthy control (both P<0.05). The Th9/Treg was higher in patients with psoriasis than that in healthy control (P<0.05). After treating CD4+ T cells with 150 ng/mL of chemerin, the levels of IL-6, IL-9 and IL-17 were increased significantly (all P<0.05). Additionally, Th9/Treg was increased (P<0.05) and the cell balance was disrupt. However, the effects of chemerin on CD4+ T cells were reversed by silencing of chemR23 (all P<0.05).
 Conclusion: Chemerin may regulate the immune balance for Th9/Treg in CD4+ T cells from patients of psoriasis.
Chemokines ; Flow Cytometry ; Humans ; Intercellular Signaling Peptides and Proteins ; Psoriasis ; T-Lymphocytes, Helper-Inducer ; T-Lymphocytes, Regulatory

B-Lymphocytes ; Graft vs Host Disease ; Humans ; Immunoglobulin D ; T Follicular Helper Cells ; T-Lymphocytes, Helper-Inducer

This study was performed to investigate the change of T-lymphocyte subsets to evaluate the immune reactivity of herpes simplex keratitis patients. Peripheral blood lymphocytes were obtained from fourteen herpes simplex keratitis patients and fourteen controls. These cells were incubated with a panel of lymphocyte specific monoclonal antibodies and then CD4+ helper and CD8+ suppressor T cells were measured by the use of flow cytometer. The following results were obtained. 1. The mean age of the control group was 46.4+/-15.9(mean+/-SD)years. The proportion of CD4+ helper T cell was 41.93 +/- 7.89%(mean +/- SD), the proportion of CD8+ suppressor T cell was 24.35 +/- 5.54% and the CD4+ helper/ CD8+ suppressor T cell ratio was 1.86 +/- 0.47. 2. The mean age of herpes simples keratitis patients was 49.9 +/- 16.4 years. In the patients, CD4+ helper/ CD8+ supressor T cell ratio was 1.25 +/- 0.42, a decrease compared to cells from controls (P<0.01). The proportion of CD4+ helper T cell was 30.1 +/- 7.11%, a decrease compared to controls(P<0.01). CD8+ suppressor T cell was 25.96 +/- 7.90%. There was no significant change in the CD8+ suppressor T cell. In this study, herpes simplex keratitis patients were accompanied by decrement in the ratio of helper to suppressor T cells and this decreased ratio was due to a decrease in helper T cells. These results suggest that cell mediated immune reactivity is depressed in herpes simplex keratitis patients.
Antibodies, Monoclonal ; Herpes Simplex* ; Humans ; Keratitis ; Keratitis, Herpetic* ; Lymphocytes ; T-Lymphocyte Subsets* ; T-Lymphocytes* ; T-Lymphocytes, Helper-Inducer

The pathogenetic mechanisms of minimal change disease and immunoglobulin A nephropathy remain uncertain, but recently various reports have reported the important role of the immunological aspect in the pathogenesis of glomerular injury. To assess the abnormalities of immunoregulatory system in these glomerular disease, the percentages of lymphocyte subpopulations in peripheral blood were studied in 24 cases of minimal change disease and 28 of immunoglobulin A nephropathy diagnosed by renal biopsy. The results were as follows: 1) CD4/CD8 ratio of the minimal change disease was significantly increased, compared with normal controls and immunoglobulin A nephropathy(P<0.05). 2) No significant difference in T helper cell and T suppressor cell was found between steroid response group and steroid non-response group in minimal change disease. 3) No significant difference in lymphocyte subpopulation was found between group with nephrotic range of proteinuria and group without nephrotic range of proteinuria in minimal change disease. 4) The discrepancies in lymphocyte subpopulations was not observed between group with infection and group without infection in immunoglobulin A nephropathy. 5) The pathologic grade (criteria of WHO) did not demonstrate a significant difference in lymphocyte subpopulation in immunoglobulin A nephropathy. In conclusion, these results suggest that the dysregulation of cell-mediated immunologic system is involved in the pathogenesis of minimal change disease and immunoglobulin A nephropathy, and some differences of immunoregulatory abnormalities between minimal change disease and immunoglobulin A nephropathy exist. But in this study the change in lymphocyte subpopulation does not anticipate the clinical course and prognosis of minimal change disease and immunoglobulin A nephropathy.
Biopsy ; Glomerulonephritis, IGA* ; Humans ; Immunoglobulin A* ; Lymphocyte Subsets* ; Lymphocytes* ; Nephrosis, Lipoid* ; Prognosis ; Proteinuria ; T-Lymphocytes, Helper-Inducer

OBJECTIVE: To explore the relation of circulating follicular helper T cell (c Tfh) changes with B cell dysfunction in MDS patients. METHODS: 20 patients diagnosed as MDS from Auguct 2015 to October 2017 were enrolled in MDS group, and 20 healthy valuntears matching in age and sex were enrolled in healthy control (HC) group. The perepheral blood in 2 groups were collected, the mononuclear cells (PBMC) from which were isolated by densily gradient contrifugation, at the same time, the serum left in isolation process was reserved for further study. The flow cytometry was used to detect the ratio of cTfh such as CD4CXCR5 T cells and its subset CD4CXCR5ICOS T cells, CD4CXCR5PD-1 T cells in PBMC, as well as the ratio of plasmablast CD19CD20CD38 B cells. The ELISA was used to detect the concentration of IgA, IgM and IgG. The differences in ratio of cTfh cells and plasmablast B cells, as well as the concentration of IgA, IgM and IgG between MDS and HC groups were compared, at the same time, the correlation of cTfh cell ratio with the plasmablast B cell ratio and the concentration of IgA, IgM and IgG in MDS patient was analyzed. RESULTS: The ratio of CD4CXCR5T, CD4CXCR5ICOST cells and CD19CD20CD38B cells and the concentration of IgA, IgM and IgG decreased in MDS patients, while the ratio of CD4CXCR5PD-1T cells increased in MDS patients. The ratio of CD4CXCR5T cells, CD4CXCR5ICOST cells positively correlated with the ratio of CD19CD20CD38B cells, as well as with the concentration of IgA, IgM and IgG in MDS patients. However, the ratio of CD4CXCR5PD-1T cells negatively correlated with the ratio of CD19CD20CD38B cells, as well as with the concentration of IgA, IgM and IgG. CONCLUSION The ratio of circulating Tfh cells and their subsets showed significant changes, that correlate with B cell dysfunction in MDS patients.
B-Lymphocytes ; Humans ; Interleukins ; Leukocytes, Mononuclear ; Myelodysplastic Syndromes ; Plasma Cells ; Receptors, CXCR5 ; T-Lymphocytes, Helper-Inducer

Various immunologic investigations of 159 patients with Behqets syndrome undertaken included; the DNCB sensitization test, total T-cells and T-cell subsets and the lymphocyte transformation test using PHA. The percentage of positive esponsiveness to DNCB decreased in the order of possible (65%), suspected (60%), incomplete (37%) and complete type (37%), The number of patients with impaired LTT was larger in the group of patients with DNCB( + ) responsiveness (seventeen of 32) than in DNCB(+) group (six of 25), There was significant impairment of cell mediated immunity in Behcets syndrome compared to normal subjects, when analyzed by the impaired LTT and decreased proportions of helper T-cells.
Behcet Syndrome* ; Dinitrochlorobenzene* ; Humans ; Immunity, Cellular* ; Lymphocyte Activation ; T-Lymphocyte Subsets ; T-Lymphocytes ; T-Lymphocytes, Helper-Inducer

OBJECTIVETo review the development of T follicular helper (TFH) cells and their role in systemic lupus erythematosus (SLE) pathogenesis, the effect of dendritic cells (DCs) on TFH cells in SLE, as well as the potential use of TFH cells as a new therapeutic target in clinical practice.

DATA SOURCESThe data used in this review were retrieved mainly from the PubMed database (1989-2013). The terms used in the literature search were "T follicular helper cells," "systemic lupus erythematosus," and "dendritic cells."

STUDY SELECTIONRelevant publications about the TFH cells development, the interaction between the TFH cells and the DCs, and the clinical applications of TFH cells were identified, retrieved, and reviewed.

RESULTSTFH cells, a novel distinct CD4+ T cell subset, are specialized in providing help to B cells in the formation of germinal centers (GCs) and long-term protective humoral immune responses. The development of TFH cells from naïve CD4+ T cell is a multistep process. As the pivot of immunoregulation, DCs are indispensable for TFH cells generation. In addition to receptor-ligand interactions between TFH cells and DCs, the cytokines secreted by DCs are also necessary for TFH cell generation. TFH cell dysregulation has been implicated in the development of SLE. More evidence from animal models of SLE and SLE patients suggests that TFH cells are necessary for pathogenic autoantibody production. Therefore, therapeutically targeting TFH cells can be a promising approach to treat antibody-mediated autoimmune diseases including SLE.

CONCLUSIONTFH cells play a critical role in the pathogenesis of SLE, making them attractive therapeutic targets in clinical practice.

No abstract available.
Animals ; Antibodies* ; Antibodies, Anticardiolipin ; beta 2-Glycoprotein I* ; Mice* ; T-Lymphocytes, Helper-Inducer*