When a nerve is injured, immune cells known as macrophages are rapidly recruited to the site. But what transforms these cells into specialized “nurses” capable of promoting nerve regeneration? The answer lies in the sophisticated dialogue between neurons and macrophages, revealed by an international study involving USP researchers and published in Immunity.
The study shows how sensory neurons use the molecule transforming growth factor-beta (TGF-β) to instruct macrophages, turning them into essential cells for nerve repair, functioning as a kind of “molecular postal code.” The research was led by Julia Kolter of the University of Freiburg (Germany) and included Brazilian scientist Conceição Elidianne Aníbal Silva and professor Thiago Mattar Cunha from the Center for Research on Inflammatory Diseases (CRID) at the Ribeirão Preto Medical School (FMRP) of USP.
The finding is significant because 2% to 3% of the world’s population suffers from neuropathies, which cause pain, weakness, and loss of sensation. Macrophages are immune cells that engulf pathogens and dead cells, but they also play vital roles in tissue repair and organ homeostasis. Transforming growth factor-beta is a multifunctional signaling molecule involved in inflammation control, scarring, and cell differentiation. It is secreted in an inactive form and becomes functional only after being locally activated.
Researchers identified a specific population of macrophages – sNAMs – that reside alongside the sensory nerves of the skin. These nerves detect touch, temperature, and pain and transmit this information to the central nervous system. Originating during embryonic development, sNAMs patrol nerves and are essential for their regeneration. After injury, blood-derived macrophages are rapidly recruited to the site and, upon making direct physical contact with nerves, convert into sNAMs that are functionally identical to the resident cells.
