Figure 3.

JNK modulates keratinocyte production of inflammatory cytokine/chemokines and recruitment of immune cells in psoriasis. Tissue damage signals (e.g., DAMPs, CCN1) activate the JNK signaling pathway in keratinocytes (KC), resulting in increased expression and release of inflammatory chemokines (e.g., CCL20, and hβD-2) and cytokines (e.g., IL-6, IL-8 IL-23, IFNγ, and TNFα). These molecules not only propagate inflammatory signals in keratinocytes, but also stimulate recruitment and activation of Th1/Th17 immune cells, which produce additional cytokines (e.g., IL-17, IL-22, and hβD-2), leading to propagated dysregulation of keratinocyte proliferation and differentiation and consequently development of psoriasis.