“What do we know about regulatory T cells and endometriosis? A systematic review”

Barros, Isabela Bottura Leite de; Malvezzi, Helena; Gueuvoghlanian-Silva, Bárbara Yasmin; Piccinato, Carla de Azevedo; Rizzo, Luiz Vicente; Podgaec, Sérgio

doi:10.1016/j.jri.2017.04.003

Cited by 69 publications

(42 citation statements)

References 58 publications

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“…These cells are regarded as important leukocytes in abdominal immunity [35] . The activated T cells move to abdominal cavity, coordinate chemokine production and leukocyte transportation and home to the adhesion sites [36] . T cells and their secreted cytokines and chemokines play pivotal roles in the initiation and development of adhesion formation [37] .…”

Section: Discussionmentioning

confidence: 99%

Effect of Ligustrazine Nanoparticles on Th1/Th2 Balance by TLR4/MyD88/NF-κB Pathway in Rats with Postoperative Peritoneal Adhesion

Yang

Lian

Zhang³

et al. 2020

Preprint

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Background Postoperative peritoneal adhesion (PPA) is regarded as fibrous bands connecting both injured abdominal wall and organs or adjacent tissues and associated with T helper (Th)1 and Th2 differentiation. However, the critical role of immunopathogenesis of adhesion formation was precisely unknown. Previously we demonstrated that ligustrazine have positive effects on adhesion formation. And microarray analysis revealed TLR4/MyD88/NF-κB pathway as an important underlying regulatory mechanism in the onset and development of PPA. To further explore the possible mechanism of PPA and enhance the specificity of ligustrazine delivery to injured sites of rodent models, a new agent polylactic acid (PLA) nanoparticles loaded with ligustrazine, that is, ligustrazine nanoparticles (LN) were applied. Methods Twenty-four SD rats were randomly divided into sham, model, LN and sodium hyaluronate (SH) groups. The structure of LN, including entrapment efficiency (EE) and loading capacity (LC), and in vitro drug release were calculated. Adhesions were scored and the masson’s trichrome staining was used to determine the collagen deposition. The expression of TLR4, MyD88 and NF-κB were measured by qPCR, Immunohistochemistry and western blot assay. Moreover, Th1-related cytokines (IFN-γ, IL-12), Th2-related cytokines (IL-4, IL-6) in the cecum tissue and serum were conducted by ELISA. Results LN had good EE, LC and control-release delivery characters with fairly uniform diameter and spherical morphology. It could effectively prevent adhesion formation after surgery. Besides, it could reduce collagen fibers accumulation, downregulate the expression levels of TLR4, MyD88 and NF-κB, and maintain Th1/Th2 balance. Conclusions Ligustrazine nanoparticles had effective effects on Th1/Th2 balance by regualtingTLR4/MyD88/NF-κB pathway in PPA rats. It may be served as a promising therapy on postoperative adhesion formation.

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Section: Discussionmentioning

confidence: 99%

Effect of Ligustrazine Nanoparticles on Th1/Th2 Balance by TLR4/MyD88/NF-κB Pathway in Rats with Postoperative Peritoneal Adhesion

Yang

Lian

Zhang³

et al. 2020

Preprint

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“…In plasma of women with endometriosis, numerous reports have identified changes in immunology (77)(78)(79)(80)(81)(82)(83)(84)(85), lymphocytes (86), prostaglandins (87), and insulin-like growth factor I (88). That the low natural killer (NK) cell activity in plasma remains low whereas the elevated CA-125 concentrations return to normal after surgical excision of deep endometriosis suggests that the NK cell defect is a cause and the elevated CA-125 a consequence of endometriosis (89).…”

Section: Other Observations Associated With Endometriosismentioning

confidence: 99%

Pathogenesis of endometriosis: the genetic/epigenetic theory

Koninckx

Ussia

Adamyan

et al. 2019

Fertility and Sterility

301

187

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Objective: To study the pathophysiology of endometriosis. Design: Overview of observations on endometriosis. Setting: Not applicable. Patient(s): None. Interventions(s): None. Main Outcome Measure(s): The hypothesis is compatible with all observations. Result(s): Endometriosis, endometrium-like tissue outside the uterus, has a variable macroscopic appearance and a poorly understood natural history. It is a hereditary and heterogeneous disease with many biochemical changes in the lesions, which are clonal in origin. It is associated with pain, infertility, adenomyosis, and changes in the junctional zone, placentation, immunology, plasma, peritoneal fluid, and chronic inflammation of the peritoneal cavity. The Sampson hypothesis of implanted endometrial cells following retrograde menstruation, angiogenic spread, lymphogenic spread, or the metaplasia theory cannot explain all observations if metaplasia is defined as cells with reversible changes and an abnormal behavior/morphology due to the abnormal environment. We propose a polygenetic/polyepigenetic mechanism. The set of genetic and epigenetic incidents transmitted at birth could explain the hereditary aspects, the predisposition, and the endometriosis-associated changes in the endometrium, immunology, and placentation. To develop typical, cystic ovarian or deep endometriosis lesions, a variable series of additional transmissible genetic and epigenetic incidents are required to occur in a cell which may vary from endometrial to stem cells. Subtle lesions are viewed as endometrium in a different environment until additional incidents occur. Typical cystic ovarian or deep endometriosis lesions are heterogeneous and represent three different diseases. Conclusion(s): The genetic epigenetic theory is compatible with all observations on endometriosis. Implications for treatment and prevention are discussed. (Fertil Steril Ò 2019;111:327-40. Ó2018 by American Society for Reproductive Medicine.) El resumen está disponible en Español al final del artículo.

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“…Usually, there is a balance between populations of regulatory T-cells (T regs ), a subgroup of helper T cells (CD4+) that act as anti-inflammatory cells, and effector or cytotoxic T-cells (CD8+); this equilibrium is required to maintain immune tolerance and to eliminate endometriotic cells. However, the high levels of E2 and the reduced P4 response influence in the elevated concentration of T regs in peritoneal fluid and in the endometriotic lesions, which decrease immune surveillance (58) and suppress the immune response, promote in this way the establishment of lesions (69). In contrast, effector T cells show a decreased activity, while helper T-cells in general are increased and participate in secreting high levels of cytokines (58,70).…”

Section: Alteration Of Immune Cell Functionmentioning

confidence: 99%

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

et al. 2020

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Endometriosis is a gynecological disorder characterized by the growth of endometrial tissue (glands and stroma) outside the uterus, mainly in the peritoneal cavity, ovaries, and intestines. This condition shows estrogen dependency and progesterone resistance, and it has been associated with chronic inflammation, severe pain, and infertility, which negatively affect the quality of life in reproductive women. The molecular mechanisms involved in the pathogenesis of endometriosis are not completely understood; however, inflammation plays a key role in the pathophysiology of the disease, mainly by altering the function of immune cells (macrophages, natural killer, and T cells) and increasing levels of pro-inflammatory mediators in the peritoneal cavity, endometrium, and blood. These immune alterations inhibit apoptotic pathways and promote adhesion and proliferation of endometriotic cells, as well as angiogenesis and neurogenesis in endometriotic lesions. It has been demonstrated that hormonal alterations in endometriosis are related to the inflammatory unbalance in this disease. Particularly, steroid hormones (mainly estradiol) promote the expression and release of pro-inflammatory factors. Excessive inflammation in endometriosis contributes to changes of hormonal regulation by modulating sex steroid receptors expression and increasing aromatase activity. In addition, dysregulation of the inflammasome pathway, mediated by an alteration of cellular responses to steroid hormones, participates in disease progression through preventing cell death, promoting adhesion, invasion, and cell proliferation. Furthermore, inflammation is involved in endometriosis-associated infertility, which alters endometrium receptivity by impairing biochemical responses and decidualization. The purpose of this review is to present current research about the role of inflammasome in the pathogenesis of endometriosis as well as the molecular role of sex hormones in the inflammatory responses in endometriosis.

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“What do we know about regulatory T cells and endometriosis? A systematic review”

Cited by 69 publications

References 58 publications

Effect of Ligustrazine Nanoparticles on Th1/Th2 Balance by TLR4/MyD88/NF-κB Pathway in Rats with Postoperative Peritoneal Adhesion

Effect of Ligustrazine Nanoparticles on Th1/Th2 Balance by TLR4/MyD88/NF-κB Pathway in Rats with Postoperative Peritoneal Adhesion

Pathogenesis of endometriosis: the genetic/epigenetic theory

Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis

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