The cells that line blood vessels from the inside work differently in each organ. In the lungs they act like a tight curtain that keeps out anything unwanted. In the liver they act like janitors, grabbing waste from the blood. In the heart they help grow new vessels. With age, these cells start to forget their specialized tasks and instead do the same thing in every organ: they switch on inflammatory signals, as if every organ were coming down with a cold.
Scientists took blood vessel cells from the lungs, kidneys, liver, heart, and brain of mice of different ages and looked at which genes were active in them. It turned out that in old mice the cells increasingly neglect their own business and increasingly show pieces of proteins to the immune system. In the lungs this is especially noticeable: the vessel walls become leaky, and what should stay inside seeps through. At the same time, fully aged cells were scarce, only about 3%. So the problems begin before the cells retire.
People used to think that vascular aging was just pipe wear and tear. Now it looks more like a loss of specialization: cells stop doing their own job and start doing someone else's. This discovery helps find ways to support blood vessels in old age so that organs stay healthy longer.
In old mice, after interferon-gamma was neutralized, MHC-II levels on the endothelium of the lungs and kidneys dropped, but MHC-I stayed unchanged. This suggests that different components of antigen presentation are regulated differently. What is more, in germ-free old mice the age-related induction of MHC genes persisted, meaning the microbiota is not an obligatory trigger of this process.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.