What is already known
The immune system has to respond to the microbiota effectively, but without causing inflammation. Previous studies have shown that commensal microbes on the skin can trigger the activation of immune cells called T cells, which help regulate local immunity. However, it remains unclear whether the skin, which is home to many microorganisms, can produce another type of immune cells, known as B cells, which are responsible for producing antibodies.
What this research adds
Researchers found that the commensal bacterium Staphylococcus epidermidis triggered the production of antibodies in the skin of adult mice. These antibodies were specific to S. epidermidis, became stronger over time and lasted for up to 200 days. The skin could produce antibodies even without prior exposure to other microbes, and transferring microbes from one mouse to another triggered similar immune responses. Antibody production didn’t depend on lymph nodes — the body’s immune centers that help regulate immune responses. Rather, the skin formed its own structures that recruit immune cells, including T and B cells.
Conclusions
The findings suggest that the skin can independently generate immune responses to control the microbiota and prevent infections, without relying on other immune centers.
The immune system has to respond to the microbiota effectively, but without causing inflammation. Now, a study in mice has revealed that the skin, which is home to many microorganisms, can independently produce long-lasting antibodies against a commensal microbe to keep its growth in check and prevent infections.
The findings, published in Nature, suggest that the skin can independently generate immune responses as a result of microbiota colonization, without relying on other immune centers.
Previous studies have shown that commensal microbes on the skin can trigger the activation of immune cells called T cells, which help regulate local immunity. However, it remains unclear whether the skin can produce another type of immune cells, known as B cells, which are responsible for producing antibodies.
To address this question, Inta Gribonika at the National Institutes of Health in Bethesda, Maryland, and her colleagues studied mice whose skin was colonized with the commensal bacterium Staphylococcus epidermidis.
Skin responses
The researchers found that S. epidermidis triggered the activity of B cells and the production of antibodies in the skin of adult mice. These antibodies were specific to S. epidermidis, became stronger over time and lasted for up to 200 days. However, colonization with S. epidermidis did not induce similar responses in newborn mice.
The skin could produce antibodies even without prior exposure to other microbes, and transferring microbes from one mouse to another triggered similar immune responses. Antibody production didn’t depend on lymph nodes — the body’s immune centers that help regulate immune responses.
Over time, there was an increase in specific T cells both in the skin and nearby lymph nodes, which suggests that the skin can generate local immune responses to keep the S. epidermidis population in check and fight off new, harmful microbes, the researchers say.
Immune autonomy
The team also found that colonization by S. epidermidis led to the formation of specialized immune structures in the skin. These structures were able to attract specific T and B cells and support the production of antibodies in response to the skin microbiota. Even in mice without lymph nodes, the skin was able to produce antibodies.
Thanks to these antibodies, mice that had been exposed to S. epidermidis were better at fighting off infections than those that had not been exposed to the microbe. These results show that the skin’s immune system can work independently to regulate microbes and protect against disease.
“Our work uncovers a new concept of skin immune autonomy, while revealing a previously unappreciated role for skin B cells in the control of host microbiota dialogue at large,” the authors say.
