The dynamics of Th17 / Treg ratio in SLE patients during pregnancy

Braga, António; Neves, Esmeralda; Guimarães, Judite; Braga, Jorge; Vasconcelos, Carlos

doi:10.1016/j.jri.2022.103622

Cited by 8 publications

(7 citation statements)

References 63 publications

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“… 27 In addition, mTORC1 facilitates the expansion of pro-inflammatory lymphocyte subpopulations in T helper 1 (Th1) and T helper 17 (Th17) cells through the regulation of hypoxia-inducible factor (HIF) −1, phosphorylation of signal transduction and transcription activator 3 (STAT3), and nuclear translocation of the transcription factor RORγt. 28 T follicular helper (Tfh) cells and Th2 cells; which drive B cell activation and autoantibody synthesis; are favored by mTORC2. 29 The transcriptional regulator FOXP3 is required for CD4 + CD25 + Treg cell activation.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Contributes to Inflammatory and Cellular Damage in Systemic Lupus Erythematosus: Cellular Markers and Molecular Mechanism

Zhu¹,

Chen²,

Xia³

2023

JIR

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Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease with complex pathogenesis, the treatment of which relies exclusively on the use of immunosuppressants. Increased oxidative stress is involved in causing inflammatory and cellular defects in the pathogenesis of SLE. Various inflammatory and cellular markers including oxidative modifications of proteins, lipids, and DNA contribute to immune system dysregulation and trigger an aggressive autoimmune attack through molecular mechanisms like enhanced NETosis, mTOR pathway activation, and imbalanced T-cell differentiation. Accordingly, the detection of inflammatory and cellular markers is important for providing an accurate assessment of the extent of oxidative stress. Oxidative stress also reduces DNA methylation, thus allowing the increased expression of affected genes. As a result, pharmacological approaches targeting oxidative stress yield promising results in treating patients with SLE. The purpose of this review is to examine the involvement of oxidative stress in the pathogenesis and management of SLE.

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Section: Introductionmentioning

confidence: 99%

Oxidative Stress Contributes to Inflammatory and Cellular Damage in Systemic Lupus Erythematosus: Cellular Markers and Molecular Mechanism

Zhu¹,

Chen²,

Xia³

2023

JIR

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“…The difference in gestational days may affected the comparisons' accuracy of Th17 cell between normal and ICP groups. However, previous and recent studies both found Th17 cell count keep stable during all pregnancy [33,34]. Additionlly, the mean gestational days in both groups was over 37 weeks.…”

Section: Discussionmentioning

confidence: 58%

Altered Expression of STAT3, RORγt, and IL-17A Proteins and Th17 Cell in Intrahepatic Cholestasis of Pregnancy

Wu¹,

Chen²,

Chen³

et al. 2022

Clin. Exp. Obstet. Gynecol.

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Background: Intrahepatic cholestasis of pregnancy (ICP) is a disorder specifically associated with pregnancy. Recent evidence suggests that the T helper 17 (Th17) cell population is related to a maternal and foetal immune imbalance associated with ICP. However, there has been insufficient attention paid to the potential roles of signal transducer and activator of transcription 3 (STAT3) and RAR-related orphan receptor gamma (RORγt) in modulations of Th17 cell in ICP. Accordingly, the purpose of our study was to investigate the alterations of Th17 cell in placenta and peripheral blood of patients with ICP and correlations between Th17 cell and STAT3, RORγt, interleukin (IL)-17A in ICP. Methods: Nine pregnant women with ICP and nine women with normal pregnancy served as the ICP and control groups, respectively. STAT3, RORγt, and IL-17A expression were examined by immunohistochemistry and western blotting in placental tissue. Flow cytometry was used to quantify Th17 cell in blood of peripheral circulation. We compared data between groups using Chi-square tests or paired t tests. Pearson or Spearman coefficients were used to measure correlations. Results: STAT3, RORγt, and IL-17A were mainly expressed in the trophoblasts of the two groups of patients. Comparatively to the control group, placental levels of STAT3, RORγt, and IL-17A proteins were significantly elevated in ICP group, as was maternal levels of Th17 cell in peripheral blood. Moreover, placental IL-17A protein level showed significantly positive relationships with placental STAT3 (r = 0.97, p = 2e-05) and RORγt (r = 0.91, p = 0.01) protein in control group, however, not in ICP group (STAT3, r = 0.5, p = 0.17; RORγt, r = 0.62, p = 0.07). Conclusions: Women with ICP showed an increase in Th17 cells in comparison to women with normal pregnancies. STAT3 and RORγt may increase Th17 cell proliferation and differentiation, appears to be altered in ICP. ICP may be adversely affected by excessive accumulation of Th17 cell.

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“…Since there is an exacerbation in the Th1 response, such a response is modulated by the Treg response, reducing the likelihood of miscarriages or pregnancy losses 12 . Additionally, the immune response profiles of Th17 and Treg mutually regulate each other thanks to the plasticity of responses in an environment of immune tolerance 13 , and differentiation between the two 14,15 . At the beginning of pregnancy, the Treg immune response profile reaches its highest levels, gradually decreasing until the moment of childbirth 13,16,17 , while the stability of Th17 13 .…”

Section: Immune Response During Pregnancy and Postpartummentioning

confidence: 99%