An interesting story about the immune system. I wonder about auto-immune risk with rejuvenated immune systems, as is being done by Greg Fahy…
The immune system is meant to protect the body from infection and disease. But with age, it can become less capable of doing so. However, Mayo Clinic researchers have found that some older people maintain “immune youth” – a new term coined by Mayo researchers to explain a young immune system in someone over age 60.
“We are studying why some individuals have a ‘fountain of youth’ in their immune systems. We want to learn from them,” says Cornelia Weyand, M.D., Ph.D., a Mayo Clinic rheumatologist and clinician-scientist. She is a lead author on a perspective paper published in Nature Aging.
“We observed that these patients have very young immune systems despite being in their 60s and 70s. But the price they pay for that is autoimmunity,” she says.
Autoimmunity is when the immune system mistakenly attacks healthy tissues and organs.
Benefits of immune system aging
“Contrary to what one may think, there are benefits to having an immune system that ages in tandem with the body,” says Jörg Goronzy, M.D., Ph.D., a Mayo Clinic researcher on aging who is a co-lead author of the paper. “We need to consider the price to pay for immune youthfulness. That price can be autoimmune disease.”
Read the full story:
Nature Article:
Sustained immune youth risks autoimmune disease in the aging host
Abstract
Immune responses underlying autoimmune diseases follow the same principles that protect individuals from infection and malignancies. However, while protective immunity wanes with progressive age, the risk for autoimmune disease steadily increases; incidence rates for many autoimmune diseases peak in later life. Here, we discuss whether aging predisposes to autoimmunity, arguing that disease progression in the autoimmune vasculitis giant cell arteritis is driven by age-inappropriate sustenance of immune competence. Stem-like memory CD4+ T cells (TSCM) that reside near the vasculitic lesions provide a continuous supply of pathogenic effector T cells. Antigen-presenting cells lacking inhibitory ligands further impede peripheral tolerance mechanisms. In the context of aging-associated accumulation of neoantigens, this incessant immune competence sets the stage for unopposed autoimmunity. We propose that sustained immune youthfulness can be detrimental to the aging host, while immune aging may be a beneficial adaptation to balance reactivity to self-antigens and non-self-antigens and thus protect from autoimmunity in aging.