The skin is the human body's largest organ and is home to a diverse and complex variety of innate and adaptive immune functions that protect against pathogenic invasion. Recent studies have demonstrated that cutaneous commensal bacteria modulated the host immune system. For example, Staphylococcus epidermidis, a skin commensal bacterium, has been demonstrated to induce cutaneous interferon (IFN)-γ- and interleukin (IL)-17A-producing T cells. In addition, cutaneous microbiota changes occur in the chronic inflammatory skin disorders, such as atopic dermatitis, and may influence the activity of skin diseases. In this article, we will review the recent findings related to the interactions of the commensal bacteria with skin homeostasis and discuss the role of the dysbiosis of these bacteria in the pathogenesis of skin diseases.