No abstract

No abstract

No abstract

Our findings support the categorization of human DSCs as non-professional APCs and suggest that PD-1 ligands on DSCs, together with major histocompatibility complex class II, may play a crucial role in the regulation of decidual CD4(+) T cell cytokine production. This helps to maintain a balanced cytokine milieu at the feto-maternal interface.

Endometriosis is a common condition with a varied phenotype. Symptomatic cases have been associated with progesterone resistance and dysregulated cytokine production in both ectopic and eutopic endometrium. In at least some cases, this seems to be associated with chronic local inflammation and antibody self-reactivity. Coexistence of endometriosis with autoimmune disease has been documented in a small number of cases, and the presence of autoreactive antibodies in the serum of some patients with endometriosis is commonly reported. This paper briefly reviews the association between endometriosis and autoimmune disease and describes the potential role of inflammation in the development of immunologic self-reactivity in these patients.

Comprehensive, nonoperative management of PFD including pelvic floor muscle training, biofeedback, electrogalvanic stimulation, constipation management, behavioral modification, incontinence devices, and pharmacotherapy including vaginal estrogen is effective in the treatment of women with PFD.

Although T cells are the most common decidual lymphocyte subset in late pregnancy, little is known about the mechanisms controlling their function. Costimulatory signaling, mediated by inducible costimulator (ICOS)-B7H2 interactions, is a known potent regulator of T-cell activation. We aimed to determine its role in fetomaternal immunity. T cells from matched peripheral blood and term decidua were assessed for ICOS, CD4/CD8, CD45RA/CD45RO and Foxp3 expression and for alterations in cytokine production upon ICOS-B7H2 ligation. We also assessed ICOS-B7H2 communication between T cells and a trophoblast cell line (JEG3). Strong ICOS expression was observed on CD4 and CD8 decidual (d)T cells, but not peripheral (p)T cells. Among dT cells, ICOS expression was higher on the predominant CD45RO + cell population compared with CD45RA + cells. Strong ICOS expression was also seen on CD4 + Foxp3 + regulatory T cells in the decidua. ICOS ligation enhanced T-cell secretion of interferongamma (IFN-c) and interleukin-10 (IL-10), but not IL-2. The impact of ICOS stimulation was more remarkable in dT cells when compared with pT cells. T cells co-cultured with JEG3 cells promoted T-cell production of IFN-c and IL-10, an effect blocked by antibody-specific masking of major histocompatibility class I or B7H2. These findings suggest that T-cell cytokine modulation by ICOS-B7H2 interactions is important in the delicate immune balance at the fetomaternal interface. The maternal endometrial lining during pregnancy is modified from the non-pregnant state and called the maternal decidua. It represents an initial contact point for genital pathogens and, therefore, has specialized innate and adaptive immune attributes. 1 This same tissue, however, must simultaneously tolerate the growing pregnancy, allowing allogenic fetally derived placental cells to reside in direct apposition with immunocompetent maternal lymphocytes. 2 CD56 bright CD16 dim natural killer (NK)-like cells (also called decidual NK cells) and CD3 + T cells comprise the two major subsets of decidual lymphocytes. 3 The number of T cells residing in the decidua throughout pregnancy is constant, although their percentage among decidual lymphocytes increases from 10-30% in the first trimester to 60-80% in the third trimester because of a significant reduction in the number of decidual (d)NK cells. 3 Although T-cell killing functions in the decidua need to be preserved throughout pregnancy to prevent expansion of localized infections, this must always be balanced by T-cell tolerance toward fetal antigens. Therefore, exquisite control of T-cell immunity and tolerance is key to successful pregnancy.Efficient T-cell activation requires both the engagement of the T-cell receptor with the major histocompatibility/antigen complex on antigen presenting cells (APCs) and the engagement of costimulatory molecules. 4 Costimulatory signaling is also delivered by ligand-receptor binding, which positively or negatively modulates the activation level of the T cell and its subsequent functional ...

HLA-G is expressed by endometriotic glandular epithelium but not by eutopic endometrium under normal conditions. Differential expression of HLA-G suggests that peritoneal inflammation or cellular stress may up-regulate mechanisms to promote ectopic endometrial survival.