CD4+CD25+ regulatory T cells (TREG) in Systemic Lupus Erythematosus (SLE) patients: The possible influence of treatment with corticosteroids

Azab, Noha A.; Bassyouni, Iman H.; Emad, Yasser; El-Wahab, G.A. Abd; Hamdy, Gehan; Mashahit, Mohammed A.

doi:10.1016/j.clim.2007.12.010

Cited by 90 publications

(58 citation statements)

References 44 publications

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“…The mean (± SD) percentages of CD4+CD25 bright as well as the total CD4+ CD25+ T cells are in line with the published "normal" values [9,16,17]. CD4+CD25+ T cells have been investigated in several autoimmune diseases, presenting conflicting results in most cases [14][15][16][17][18][19][20][21][22]. These discrepancies may be attributed to the differences in the selection of patients (active or inactive diseases) or probably due to technical difficulties in CD4+ CD25+ T cells phenotypic characterization.…”

Section: Fig (2) Percentages Of Cd4+ Cd25supporting

confidence: 85%

“…Because CD25 is transiently up-regulated in T cells after activation, circulating CD4+CD25+ T cells make a heterogeneous population [27]. Furthermore, patients treated with corticosteroids, alone or with other immunosuppressive drugs, had a significantly higher level of CD4+CD25+ than the group of patients not on corticosteroids treatment and the control group [14]. Our groups of patients were all in immunosuppressive drugs including corticosteroid.…”

Section: Fig (2) Percentages Of Cd4+ Cd25mentioning

confidence: 82%

“…A recent study done by Azab et al showed that the levels of CD4+CD25+ % T cells in SLE patients were higher than in the control group, but it was statistically insignificant [14]. Also Suárez et al [15] found no significant difference of CD4+CD25+ % T cells between SLE patients and control group.…”

Section: Introductionmentioning

confidence: 92%

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Quantification of CD4' CD25' Regulatory T Cells in Peripheral Blood of Patients with Systemic Lupus Erythematosus and Rheumatoid Arthritis

Al-Shukaili¹,

Alkaabi²,

Al-Gafri³

et al. 2009

TOAUTOJ

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Recent animal studies have shown that regulatory T cells play a crucial role in the suppression of the immune response and that depletion of this subset of T cells might lead to development of autoimmune diseases. The aim of this work was to quantify regulatory T cells (CD4+ CD25+) in the peripheral blood of Omani patients with Systemic Lupus Erythematosus (SLE) and Rheumatoid arthritis (RA) and correlate these findings with the disease activity of the patients. Thirty patients with SLE, 30 patients with RA and 25 healthy volunteers were enrolled in this study. Patients were divided into highly active or low active groups, depending on the disease activity. Flow cytometer was used to quantify CD4+ CD25+ T cells in the peripheral blood mononuclear cells (PBMC). We found that both highly active SLE (0.242 ± 0.3) and RA (0.56 ± 0.29) patients had significantly (p<0.001) lower levels of CD4+CD25 bright T cells than did normal controls (1.74 ± 0.47%) or patients with low disease activity (SLE=1.54 ± 0.33, RA=1.829 ± 0.76). The decreased number of CD4+CD25 bright T cells during disease activity was restored in remitting phase of SLE patients. This data provides further evidence supporting the hypothesis of defect of regulatory T cells in SLE and RA patients; which may have an important implication in the context of the control of the inflammation and development of autoimmunity.

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Section: Fig (2) Percentages Of Cd4+ Cd25supporting

confidence: 85%

Section: Fig (2) Percentages Of Cd4+ Cd25mentioning

confidence: 82%

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Quantification of CD4' CD25' Regulatory T Cells in Peripheral Blood of Patients with Systemic Lupus Erythematosus and Rheumatoid Arthritis

Al-Shukaili¹,

Alkaabi²,

Al-Gafri³

et al. 2009

TOAUTOJ

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“…Our previous study showed that there is a significant increase in Treg numbers in SLE patients in Indonesia compared to a healthy control (10). Similar phenomenon showing a significant increase in the Treg numbers were also shown in other studies (11)(12)(13). Despite these contradictory results of the role of Tregs in SLE, better knowledge about Tregs will not only provide new insights into the pathogenesis of SLE but also can be used to develop various clinical applications, including preventive and curative treatment for SLE.…”

Section: Introductionsupporting

confidence: 76%

Regulatory T Cells Compensation Failure Cause the Dysregulation of Immune Response in Pristane Induced Lupus Mice Model

Kalim

Pratama

Nugraha

et al. 2018

MJMS

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Introduction: Regulatory T cells' (Tregs') role remains unclear in the pathogenesis of systemic lupus erythematosus (SLE). This study was aimed at monitoring the percentage of Tregs within 32 weeks and monitoring its relationship with the percentage of other T helper (Th) cell subsets and the levels of autoantibodies and pro-inflammatory cytokines in a murine SLE model induced by pristane.Methods: Forty-eight female BALB/c mice were divided into a healthy control (HC) and a pristine-induced (PI) group. SLE was induced by a single 0.5 cc pristane intraperitoneal injection. Six from each group were sacrificed every eight weeks until 32 weeks post-pristane injection. Treg, Th1, Th2 and Th17 percentages from the spleen were measured using flowcytometry. ANA, IL-6 and IFN-α levels were measured from serum using ELISA.Results: The Treg percentage from the PI group increased significantly at 16 weeks compared to the HC group, while Th1, Th2 and Th17 percentages decreased. Tregs in the PI group began to reduce from the 24th to 32nd weeks, followed by an elevation of the Th1, Th2 and Th17 percentages. Tregs were negatively correlated with Th1 and Th2. Tregs in the PI group had a negative correlation with ANA and IFN-α levels from serum, whereas Tregs had a positive correlation with IL-6 levels.Conclusion: The compensation of Tregs observed at 16 weeks after pristane injection failed, marked by a decreasing number of Tregs, followed by an increase of Th subsets, proinflammatory cytokines and autoantibodies. This compensatory failure of Tregs could be affected by pro-inflammatory cytokines, such as IFN-α and IL-6.

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“…Recent research has confirmed that the frequency and function of Treg cells are deficient in patients with active SLE (32) but could be restored by corticosteroid treatment inducing disease remission (33), suggesting a role for this T cell subset in the pathogenesis of human SLE. The transcription factor FoxP3 acts as a crucial molecule in Treg cell development and function and is widely used as a nuclear marker for Treg cells (34).…”

Section: Discussionmentioning

confidence: 97%

Umbilical cord mesenchymal stem cell transplantation in severe and refractory systemic lupus erythematosus

Sun

Wang

Liang

et al. 2010

Arthritis & Rheumatism

425

310

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Objective. Umbilical cord (UC)-derived mesenchymal stem cells (MSCs) have shown marked therapeutic effects in a number of diseases in animal studies, based on their potential for self-renewal and differentiation. No data are available on the effectiveness of UC MSC transplantation (MSCT) in human autoimmune disease. This study was undertaken to assess the efficacy and safety of allogeneic UC MSCT in patients with severe and treatment-refractory systemic lupus erythematosus (SLE).Methods. We conducted a single-arm trial that involved 16 SLE patients whose disease was refractory to standard treatment or who had life-threatening visceral involvement. All of the patients gave consent and underwent UC MSCT. Clinical changes were evaluated before and after transplantation using the SLE Disease Activity Index (SLEDAI), measurement of serum antinuclear antibody (ANA), anti-double-stranded DNA (anti-dsDNA) antibody, serum complement C3 and C4, and albumin levels, and assessment of and renal function. Evaluation of potential mechanisms of MSCT effects focused on the percentage of peripheral blood Treg cells and serum levels of cytokines.Results. From April 2007 to July 2009, a total of 16 patients with active SLE were enrolled and underwent UC MSCT. The median followup time after MSCT was 8.25 months (range 3-28 months). Significant improvements in the SLEDAI score, levels of serum ANA, anti-dsDNA antibody, serum albumin, and complement C3, and renal function were observed. Clinical remission was accompanied by an increase in peripheral Treg cells and a re-established balance between Th1-and Th2-related cytokines. Significant reduction in disease activity was achieved in all patients, and there has been no recurrence to date and no treatment-related deaths.Conclusion. Our findings indicate that UC MSCT results in amelioration of disease activity, serologic changes, and stabilization of proinflammatory cytokines. These data provide a foundation for conducting a randomized controlled trial of this new therapy for severe and treatment-refractory SLE.Systemic lupus erythematosus (SLE) is an inflammatory disease with protean manifestations, ranging from relatively minor skin and joint symptoms to severe life-threatening major organ involvement, such as nephritis and neuropsychiatric complications (1). It is characterized by the presence of autoreactive T and B lymphocytes, with polyclonal activation of B cells and the consequent production of autoantibodies by plasma ClinicalTrials.gov identifier: NCT00698191.

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CD4+CD25+ regulatory T cells (TREG) in Systemic Lupus Erythematosus (SLE) patients: The possible influence of treatment with corticosteroids

Cited by 90 publications

References 44 publications

Quantification of CD4' CD25' Regulatory T Cells in Peripheral Blood of Patients with Systemic Lupus Erythematosus and Rheumatoid Arthritis

Quantification of CD4' CD25' Regulatory T Cells in Peripheral Blood of Patients with Systemic Lupus Erythematosus and Rheumatoid Arthritis

Regulatory T Cells Compensation Failure Cause the Dysregulation of Immune Response in Pristane Induced Lupus Mice Model

Umbilical cord mesenchymal stem cell transplantation in severe and refractory systemic lupus erythematosus

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