ABSTRACT
Psoriasis is a chronic immune-inflammatory disease predominantly affecting skin and joints. Neutrophils are the key effectors in the inflammation in psoriasis. Stress, microbial dysbiosis, and so forth, lead to keratinocyte dysfunction and subsequent production of pro-inflammatory cytokines like TNF-α, IL-23, IL-12, and IFN-α by dendritic cells. IL-23 in turn acts on IL-17, producing T cells and innate immune cells, and causes production of IL-17 and IL-22. These cause keratinocyte proliferation and neutrophilic infiltration. Therapies targeted at the IL-23/IL-17 axis have shown excellent results, confirming the major role of this pathway in inflammation.
