Yale study reveals battle formation of immune cell soldiers in skin

The skin is the body’s first line of defense against potential infection, and new research has brought us closer to understanding how it works. Researchers at Yale have now identified how immune cells spread themselves out to maintain the most effective patrol.

The epidermis is the outermost layer of skin, and its primary function is to act as a barrier to the outside world. That’s not just a physical barrier either – the immune system deploys certain cells throughout the epidermis to act as bouncers and keep the bad bugs out.

In the new study, researchers from Yale and Michigan State University investigated how two types of these immune cells – Langerhans cells and dendritic epidermal T cells (DETCs) – interact with the skin cells, or epithelial cells, around them to maintain that barrier.

These immune cells are known to spread out wide, avoiding clustering together to keep watch most efficiently. The new study confirmed this by removing some of these cells from one area of the epidermis, and found that others would shuffle in to fill the gap in the defenses.

But how exactly the cells regulate this and maintain a consistent distribution has puzzled scientists. In the new study, the team traced it to a gene called Rac1, which regulates dendrites – the spindly protrusions on immune cells and neurons. In the latter, dendrites help neurons avoid each other to prevent clustering, and the team wondered if a similar process was occurring in immune cells.

Sure enough, when the scientists knocked out this gene, they found that the distribution of the cells was interrupted. Based on these experiments, and images of the immune system cells interacting with the epithelial cells, the researchers concluded that the distribution patterns of the two types of immune cells is regulated by both the Rac1 gene and the density of the epithelial cells around them.

“It’s a surveillance system with two separate roles,” says Catherine Matte-Martone, co-first author of the study. “The skin controls the sentinels by mediating their numbers based on its own density, while they in turn provide dynamic coverage to prevent cracks in the skin’s defenses.”

The study provides some interesting new insights into some poorly understood mechanisms that keep us safe from infection, and could eventually open up new leads on ways to boost immune responses.

The research was published in the journal Nature Cell Biology.

Source: Yale University