A Model to Demonstrate the Excessive T Cell Expansion and Differentiation of an Aged Immune System Produces Chronic Inflammation in Tissues

Researchers here use a novel model to demonstrate that T cells made to exhibiting the greater replication and differentiation characteristic of an aged immune system, leading to cellular senescence, cause chronic inflammation in heart tissue in young animals. The age-related decline of the adaptive immune system is thus sufficient to cause this sort of issue in and of itself, independently of other contributing causes, leading to tissue dysfunction. Clearing out harmful immune cells via senolytic drugs or other targeted approaches is one option, but a source of replacement T cells is also needed. A large part of the dysfunction of the aged adaptive immune system arises because the thymus, where T cells mature, atrophies in later life. Medical development must focus on at least two goals: restoring the thymus and selectively destroying harmful T cells. The cardiovascular and immune systems undergo profound and intertwined alterations with aging. Recent studies have reported that an accumulation of memory and terminally differentiated T cells in elderly subjects can fuel myocardial aging and boost the progression of heart diseases. Nevertheless, it remains unclear whether the immunological senescence profile is sufficient to cause age-related cardiac deterioration or merely acts as an amplifier of previous tissue-intrinsic damage. Herein, we sought to clarify the causality in this cardio-immune crosstalk by studying young mice harboring a senescent-like expanded...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs