The many faces of interleukin-17 in inflammatory skin diseases

Abstract

Interleukin (IL)-17 is an emerging target for inflammatory skin disorders. Given the remarkable success of its therapeutic inhibition in psoriasis, the pathogenic role of this cytokine is being explored in other immune-mediated diseases. Interestingly, IL-17 is linked to particular skin conditions where its activation coincides with disease flares. The leading hypothesis for its contribution to proinflammatory signalling cascades is driving inflammasome activation. However, IL-17 stimulation also releases a range of noninflammasome-related cytokines from human skin. Furthermore, a role in cytotoxic responses and an important interplay with the microbiome is hypothesized. While treatment failure would be surprising in neutrophilic dermatoses, the picture might be more complex in lymphocyte-mediated conditions. Nonetheless, increasing insights into the pathogenesis suggest that beneficial responses are also probable in the latter conditions. Study of this pathway in the skin reveals some intriguing aspects of the IL-17-related immunological network.

Different expression patterns of plasma Th1‐, Th2‐, Th17‐ and Th22‐related cytokines correlate with serum autoreactivity and allergen sensitivity in chronic spontaneous urticaria

“…10 A complex network of cytokines released by the Th cells is involved in various autoimmune and allergic responses. 15 IL-22 is synthesized and released by Th22, and both IL- 22 and Th22 have been confirmed to play important roles in atopic diseases. 12 The imbalance between Th1 and Th2 has long been considered as a possible mechanism in urticaria.…”

Gold lotion from citrus peel extract ameliorates imiquimod‐induced psoriasis‐like dermatitis in murine

“…Subsequently, a functional role of IL‐23/Th17 in the immunopathogenesis of psoriasis was demonstrated . Th17 cells are inflammatory Th cells characterized by the expression of IL‐17A/F, IL‐21, IL‐22, and potentially TNF‐α and IL‐6, and a high level of retinoic acid‐related orphan receptors (RORα and RORγ) . Although Th17 cells were originally regarded as the major source of IL‐17 in psoriasis, accumulating evidence suggests that other innate immune cell types, including γδ T cells, innate lymphoid cells (ILCs), NKT cells, and neutrophils, can also produce IL‐17 .…”

Major Depression and Psoriasis: A Psychodermatological Phenomenon

“…The authors calculated the blood BDNF levels instead of brain BDNF levels and found that these BDNF levels are reduced in depression and psoriasis. Abnormal IL-17 expression has also been observed in psoriatic patients with therapeutic inhibition showing success in reducing disease severity [35,36]. Furthermore, as has been discussed above, inflammatory cytokines like TNF-α, IFN-γ, and other type-1 cytokines play a crucial part in the pathophysiology of psoriasis [26].…”