Macrophages (Greek: big eaters, from Greek μακρος (makros) = large, φαγειν (phagein) = to eat) are white blood cells that engulf and digest cellular debris, foreign substances, microbes, cancer cells, and anything else that does not have the protein markers specific to healthy body cells on its surface. This process is called phagocytosis.

Macrophages are large phagocytes and are found in all tissues, where they patrol for potential pathogens and cellular waste to dispose of.

Macrophages have a number of tissue-specific variants throughout the body (e.g., microglia, histiocytes, osteoclasts, Kupffer cells, and others), but all of them are part of the mononuclear phagocyte system and perform essentially the same housekeeping role within the body.

Macrophages develop in the bone marrow as monocytes, which circulate in the bloodstream until they settle in the tissues and become one of the many tissue-specific types of macrophage.

Besides phagocytosis, macrophages play a critical role in nonspecific defense (innate immunity) and help initiate specific defense mechanisms (adaptive immunity) by recruiting other immune cells, such as lymphocytes, to help them fight pathogens. In humans, dysfunctional macrophages cause severe diseases, such as chronic granulomatous disease, that result in frequent infections; aging causes macrophages to become increasingly poor at cellular housekeeping and fighting pathogens.

A number of research efforts have focused on trying to return aged, dysfunctional macrophages to more youthful levels of function by modulation of the immune system (in particular microglia – macrophages) using pro-youthful signalling.

One such effort in 2016 sent mesenchymal stem cells to the area of damage and resulted in a reduction of plaques in Alzheimer’s mice, as these stem cells reduce inflammation and encourage pro-youthful function via intracellular signaling [1].

Recently, researchers showed that delivering fresh, functionally young macrophages to the brain results in removal of the plaques (misfolded proteins) associated with Alzheimer’s disease [2].

This means that brain aging is not a one-way process and suggests that we might be able to use our own rejuvenated macrophages to treat this horrific disease and other, similar diseases, including heart disease and Parkinson’s, which also involve plaque accumulation.


Introducing youthful macrophages and boosting their efficiency represents a plausible pathway to treating age-related diseases, and the research world is currently investigating the potential of a number of therapies that do this.


[1] Naaldijk, Y., Jaeger, C., Fabian, C., Leovsky, C., Blüher, A., Rudolph, L., … & Stolzing, A. (2016). Effect of systemic transplantation of bone marrow‐derived mesenchymal stem cells on neuropathology markers in APP/PS1 Alzheimer’s mice. Neuropathology and applied neurobiology.

[2] Daria, A., Colombo, A., Llobera, G., Hampel, H., Willem, M., Liesz, A., … & Tahirovic, S. (2016). Young microglia restore amyloid plaque clearance of aged microglia. The EMBO Journal, e201694591.

About the author

Steve Hill

As a scientific writer and a devoted advocate of healthy longevity and the technologies to promote them, Steve has provided the community with hundreds of educational articles, interviews, and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity reporter, Psychology Today and Singularity Weblog. He is a co-author of the book “Aging Prevention for All” – a guide for the general public exploring evidence-based means to extend healthy life (in press).
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