The role of Th17 and Treg cells in normal pregnancy and unexplained recurrent spontaneous abortion (URSA): New insights into immune mechanisms

Tang, Chunbo; Hu, Wanqin

doi:10.1016/j.placenta.2023.08.065

Cited by 4 publications

(2 citation statements)

References 43 publications

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“…However, if this immune response becomes uncontrolled in later pregnancy, it can lead to miscarriage. 38 In URSA patients, there is evidence of an increased number of decidual Th17 cells and a decreased level of Tregs, indicating an imbalance in the Th17/Treg ratio likely contributes to URSA. 39 Chang et al also reported the expansion and functions of Th17 cells are regulated by CaMK4, inhibition of which can reverse the immune imbalance along the maternal-fetal interface and improve pregnancy outcomes.…”

Section: Regulation Of Decidual Immune Cells By Trophoblastsmentioning

confidence: 98%

Maternal‐fetal immunity and recurrent spontaneous abortion

Yao,

Ye,

Chen

et al. 2024

American J Rep Immunol

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Recurrent Spontaneous Abortion (RSA) is a common pregnancy complication, that has multifactorial causes, and currently, 40%–50% of cases remain unexplained, referred to as Unexplained RSA (URSA). Due to the elusive etiology and mechanisms, clinical management is exceedingly challenging. In recent years, with the progress in reproductive immunology, a growing body of evidence suggests a relationship between URSA and maternal‐fetal immunology, offering hope for the development of tailored treatment strategies. This article provides an immunological perspective on the pathogenesis, diagnosis, and treatment of RSA. On one hand, it comprehensively reviews the immunological mechanisms underlying RSA, including abnormalities in maternal‐fetal interface immune tolerance, maternal‐fetal interface immune cell function, gut microbiota‐mediated immune dysregulation, and vaginal microbiota‐mediated immune anomalies. On the other hand, it presents the diagnosis and existing treatment modalities for RSA. This article offers a clear knowledge framework for understanding RSA from an immunological standpoint. In conclusion, while the “layers of the veil” regarding immunological factors in RSA are gradually being unveiled, our current research may only scratch the surface. In terms of immunological etiology, effective diagnostic tools for RSA are currently lacking, and the efficacy and safety of immunotherapies, primarily based on lymphocyte immunotherapy and intravenous immunoglobulin, remain contentious.

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Section: Regulation Of Decidual Immune Cells By Trophoblastsmentioning

confidence: 98%

Maternal‐fetal immunity and recurrent spontaneous abortion

Yao,

Ye,

Chen

et al. 2024

American J Rep Immunol

View full text Add to dashboard Cite

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“…Notably, gestation usually protects against autoimmune diseases [ 170 , 171 ] by developing an immune-tolerant condition in which the maternal immune system adapts to the allogeneic tissues of the fetus. Cytokines produced by the fetoplacental unit can modulate maternal immune responses, promoting a strong Th2 and decreasing Th1/Th17-mediated response to reduce the risks of miscarriage [ 172 , 173 ]. Estrogen/estrogen receptor (E2/ER) signaling plays an active role in the development, differentiation, and functionality of both innate and adaptive immune cells [ 174 , 175 , 176 ].…”

Section: Sexual Dimorphism In Immunity Modulationmentioning

confidence: 99%

The Impact of Microbiota–Immunity–Hormone Interactions on Autoimmune Diseases and Infection

Martinelli,

Nannini,

Cianchi

et al. 2024

Biomedicines

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Autoimmune diseases are complex multifactorial disorders, and a mixture of genetic and environmental factors play a role in their onset. In recent years, the microbiota has gained attention as it helps to maintain host health and immune homeostasis and is a relevant player in the interaction between our body and the outside world. Alterations (dysbiosis) in its composition or function have been linked to different pathologies, including autoimmune diseases. Among the different microbiota functions, there is the activation/modulation of immune cells that can protect against infections. However, if dysbiosis occurs, it can compromise the host’s ability to protect against pathogens, contributing to the development and progression of autoimmune diseases. In some cases, infections can trigger autoimmune diseases by several mechanisms, including the alteration of gut permeability and the activation of innate immune cells to produce pro-inflammatory cytokines that recruit autoreactive T and B cells. In this complex scenario, we cannot neglect critical hormones’ roles in regulating immune responses. Different hormones, especially estrogens, have been shown to influence the development and progression of autoimmune diseases by modulating the activity and function of the immune system in different ways. In this review, we summarized the main mechanisms of connection between infections, microbiota, immunity, and hormones in autoimmune diseases’ onset and progression given the influence of some infections and hormone levels on their pathogenesis. In detail, we focused on rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus.

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