Disease susceptibility implications of preferential inactivation of the paternal X chromosome in extraembryonic endoderm of the mouse.

In the mouse, there is preferential inactivation of the paternally-derived X chromosome in extraembryonic tissues of early embryos, including trophectoderm and primitive endoderm or hypoblast. Although derivatives of these tissue have long been considered to be purely extraembryonic in nature, recent studies have shown that hypoblast-derived cells of the 'extraembryonic' visceral endoderm make a substantial cellular contribution to the definitive gut of the fetus. This raises questions about the eventual fate of these cells in the adult and potential disease implications due to the skewed inactivation of the paternally derived X in females heterozygous for X-linked mutations.

Interferon-gamma driven elevation of CXCL9: a new sepsis endotype independently associated with mortality.

Background: Endotype classification becomes the cornerstone of understanding sepsis pathogenesis. Macrophage activation-like syndrome (MALS) and immunoparalysis are the best recognized major endotypes, so far. Interferon-gamma (IFNγ) action on tissue macrophages stimulates the release of the cytotoxic chemokine CXCL9.