Skin immunity: nuances that were not known before

The skin is the primary surface of interaction between the organism and the environment. This organ is a habitat for trillions of microorganisms that play an important role in tissue homeostasis and local immunity. Skin microbial communities are very diverse. They may change over time or as a result of changing environmental conditions. How, in the context of such complexity, individual opportunistic microorganisms can differentially reduce skin immunity, as well as what are the consequences of such reactions for tissue physiology, is still unknown.

Recent research by scientists has shown that certain opportunistic pathogens primarily affect skin immunity and have identified the cellular mediators involved in this specification. In particular, colonization with Staphylococcus epidermidis stimulates IL-17A+ CD8+ T cells, enhances natural immunity and limits pathogenic invasion. The T-cell immune response to certain opportunistic pathogens results from the coordinated action of subpopulations of dendritic cells that are present in the skin and are not associated with inflammation. The cells that are in the skin respond to changes in microbial communities.

This interaction may represent an evolutionary means by which skin immunity uses fluctuating signals from opportunistic pathogens to improve the immune barrier and provide heterologous protection against pathogens.

Research findings suggest that skin immunity is a highly dynamic environment that can be rapidly and differently modified in the event of exposure to certain opportunistic pathogens. This allows us to expand the boundaries of understanding the action of tissue-specific immunity and the effect of pathogens on the skin.

Scientists believe that this information about the characteristics of skin immunity allows us to understand why the treatment of certain skin diseases (for example, acne) with antibiotics, acids, and even retinoids is not suitable for everyone.

According to http://www.nature.com/