In this thesis, I will discuss some of my recent articles that clarify the role of T helper (Th)17 and Th22 lymphocytes in two diseases presenting, among others, a state of chronic skin inflammation: systemic sclerosis (SSc) and psoriasis. SSc is characterized by an uncontrolled fibroblast response leading to dermal fibrosis. Psoriasis is characterized by an abnormal response of keratinocytes, leading to epidermal modifications. I will first refer to our discovery of the aryl hydrocarbon receptor as a priming factor of human skin-homing T cells expressing IL-22 (Th22 cells). I will next introduce the dermal dimension of Th22/Th17-mediated cutaneous inflammation, showing how these cells participate to the inflammatory component of SSc while rather restraining fibrosis. Finally, I will discuss the epidermal dimension of IL-17-mediated inflammation in psoriasis, showing that IL-17E, an IL-17A isoform, favors the recruitment of neutrophils in the skin. This will lead to the discussion of future research, including the use of human skin reconstituted models to study the epidermal-dermal communication during cutaneous inflammation.