Type 2 immunity acts as a brake on chronic inflammation in aging
Chronic low-grade inflammation is one of the most discussed features of aging. But the body also has a counterweight: mechanisms that restrain that inflammation. A new perspective piece in Nature Aging argues that this restraining system weakens as we age.
Type 2 immunity is a branch of the immune system classically linked to allergies and defence against parasites. But the authors argue in Nature Aging that it also plays a regulatory role, keeping the production of blood cells, the function of macrophages (the immune system’s waste-clearing cells), and metabolism in balance.
Aging undermines the restraining system
As we age, type 2 immune activity declines. This removes the braking effect on chronic inflammation. The authors suggest this contributes to what researchers call inflammaging: a chronic, low-grade inflammatory state characteristic of aging that is associated with conditions including dementia, diabetes, and cardiovascular disease.
It is important to note that this is a perspective article, not an experimental study. The authors present a hypothesis based on existing literature. They propose that type 2 immunity could be a target for therapies aimed at restoring immune balance in aging.
Targeting the brake on inflammaging
If the decline of type 2 immunity indeed contributes to inflammaging, restoring that immune branch could represent a new treatment direction. This remains speculative; no clinical trials have yet tested this in humans. But it offers a new framework for thinking about age-related inflammation, distinct from the common approach of suppressing inflammatory mediators.
Search terms for further reading: type 2 immunity inflammaging, immune homeostasis age-related inflammation, macrophage regulation aging