Abstract
T helper-17 (Th17) cells, which mainly produce IL-17, are associated with development of various autoimmune diseases such as rheumatoid arthritis, inflammatory bowel diseases, multiple sclerosis, and psoriasis. IL-17 and related cytokines are therapeutic targets of these diseases. In atopic dermatitis (AD), Th2 cytokines such as IL-4 and IL-13 are regarded to be the main player of the disease; however, Th17 cytokines are also expressed in AD skin lesions. Expression of IL-22 rather than IL-17 is predominant in AD skin, which is contrary to cytokine expression in psoriasis skin. Relatively low IL-17 expression in AD skin can induce relatively low antimicrobial peptide expression, which may be a reason why bacterial infection is frequently seen in AD patients. Failure of clinical trials for investigating the efficacy of anti-IL-12/23 p40 in AD has suggested that IL-17 expressed in skin lesions should not be the main player but a bystander responding to barrier dysfunction.
Highlights
Atopic dermatitis (AD) is a chronic skin disease characterized by relapsing eczema with pruritus as a primary lesion
If antibodies against T helper-17 (Th17) cytokines are not useful for AD, what is the best therapeutic target? Th2-type immune responses induced by allergens such as mites and pollen are associated with worsening of AD skin conditions
It is true that Th17 cells infiltrate into lesional skin of AD, and Th17-related cytokines are expressed there
Summary
Atopic dermatitis (AD) is a chronic skin disease characterized by relapsing eczema with pruritus as a primary lesion. Some patients develop AD in their adulthood, onset of AD in elderly people is very rare. Other skin diseases such as cutaneous T-cell lymphoma (CTCL), drug eruption, and bullous diseases should be considered as a possible diagnosis. It was reported that Th1 cytokines like interferon (IFN)-γ were expressed in AD lesional skin [14,15]. Th17 cytokines such as IL-17 and IL-22 were reported to be expressed in AD lesional skin [16,17,18,19,20]. The importance of Th17-related cytokines in pathogenesis and treatment of AD will be discussed
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