[Developmental and environnemental origin of male infertility: role of endocrine disruptors].

Human and wildlife exposure to chemicals is thought to be extensive and particularly to endocrine-disrupting chemicals (EDCs) suspected to alter male reproductive tract. When the exposure occurs during perinatal period (fetal, neonatal periods or puberty) the reproductive health alterations are irreversible suggesting a developmental origin to male infertility. This concept is supported by numerous epidemiologic and experimental studies.

Defects in mitophagy promote redox-driven metabolic syndrome in the absence of TP53INP1.

The metabolic syndrome covers metabolic abnormalities including obesity and type 2 diabetes (T2D). T2D is characterized by insulin resistance resulting from both environmental and genetic factors. A genome-wide association study (GWAS) published in 2010 identified TP53INP1 as a new T2D susceptibility locus, but a pathological mechanism was not identified.

Bone marrow Th17 TNFα cells induce osteoclast differentiation, and link bone destruction to IBD.

Objective: Under both physiological and pathological conditions, bone volume is determined by the rate of bone formation by osteoblasts and bone resorption by osteoclasts. Excessive bone loss is a common complication of human IBD whose mechanisms are not yet completely understood. Despite the role of activated CD4(+) T cells in inflammatory bone loss, the nature of the T cell subsets involved in this process in vivo remains unknown.