Publications by authors named "Lisette de Vogel"
Background: HLA-G is a nonclassical MHC class I molecule and its physiological expression restricted to placental extravillous trophoblasts contributes to maternal tolerance to the semiallogeneic fetus. Aberrant expression of HLA-G in human organ grafts has been proposed to contribute to graft acceptance.
Methods: We studied HLA-G expression in liver tissue and serum of adult liver transplant recipients before, early, and late after transplantation in relation to liver function and operational tolerance.
Background: Encapsulating peritoneal sclerosis (EPS) is a severe complication of peritoneal dialysis (PD). Previously, it has been shown that infiltrating CD4-positive T cells and M2 macrophages are associated with several fibrotic conditions. Therefore, the characteristics of the peritoneal cell infiltrate in EPS may be of interest to understand EPS pathogenesis.
View Article and Find Full Text PDFObjectives: Interferons (IFNs) have several anticancer mechanisms. A number of clinical trials have been conducted regarding adjuvant IFN-α therapy in pancreatic cancer. Type I IFNs exert their effect via the type I IFN receptor (IFNAR-1, IFNAR-2c).
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- Researchers investigated the link between specific gene polymorphisms and the risk and severity of rheumatoid arthritis (RA), focusing on various inflammatory response genes.
- They genotyped selected genes in 376 RA patients and 463 healthy controls, finding that the IL8 781 CC genotype was associated with earlier onset of RA.
- The study suggests a potential role for genetic variations in immune response related to RA, but emphasizes the need for more extensive research to clarify these connections.
Objective: Rheumatoid arthritis is associated with the infiltration of T helper cells into the joints. It is unclear whether interferon-gamma (IFNgamma)-producing Th1 cells or the novel T helper subset, interleukin-17 (IL-17)-producing Th17 cells, are the pathogenic mediators of joint inflammation in chronic nonautoimmune arthritis. Therefore, this study was aimed at examining whether the Th2-specific transcription factor GATA-3 can regulate arthritis, in an experimental murine model, by modulating Th1 and/or Th17 cell polarization.
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