It is often said that as we age, we catch colds more easily and recover more slowly. This phenomenon of weakened immunity is accepted as a 'natural result of aging.' However, research has shown that a specific biological mechanism involving the decrease of certain proteins is involved in the weakening of immunity due to aging.
According to reports from scientific media such as Science Daily, a team led by Professor Sandra Pinho from the Department of Pharmacology and Regenerative Medicine at the University of Illinois at Chicago (UIC) has confirmed that a protein called 'platelet factor 4 (PF4)' decreases during the aging process, leading to a rapid decline in the function of hematopoietic stem cells, which are the foundation of blood and the immune system. This research was published in a recent issue of the international hematology journal ⟪Blood⟫.
Hematopoietic stem cells exist in the bone marrow and are key cells that produce all blood cells, including red blood cells, as well as lymphatic immune cells such as T cells and B cells. In youth, these cells are produced in a balanced manner, maintaining stable blood and immune function.
However, as aging progresses, the differentiation of stem cells gradually shifts towards myeloid cells, and the production of lymphatic immune cells, which are crucial for responding to infections, decreases. This change is associated with the decline in immune function in the elderly and is known to be one of the reasons why older individuals are limited as bone marrow transplant donors.
The research team analyzed mouse models and human bone marrow samples and revealed that platelet factor 4 is an important signaling molecule that regulates the division frequency of hematopoietic stem cells. In young individuals, PF4 suppresses excessive division of stem cells, maintaining the stability of cell function.
In contrast, as we age, the amount of PF4 produced in immune cells decreases. As a result, stem cells divide more frequently, increasing the likelihood of accumulating genetic mutations during this process. The research team explained that these changes could be associated with chronic inflammation, increased risk of blood cancers, and cardiovascular diseases.
The research team also confirmed the changes that occur when PF4 is replenished. After administering PF4 to aged mice for more than a month, the functions and characteristics of blood and immune cells became similar to those of young individuals. Improvements in cell function were also observed when PF4 was treated in cultured aged human hematopoietic stem cells.
However, the research team emphasized that one protein, platelet factor 4, should not be expected to reverse systemic aging or extend human lifespan. Professor Pinho stated, "PF4 is not a universal key to solving the aging of all tissues, but it presents a new research direction to address age-related changes in blood and the immune system."
