1. Psoriasis pathogenesis and the development of novel targeted immune therapies 
Jason E. Hawkes, MD, Tom C. Chan, MD, PhD, James G. Krueger, MD, PhD 
Journal of Allergy and Clinical Immunology 
Volume 140, Issue 3, Pages (September 2017)
DOI: /j.jaci
Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2. Fig 1
IL-23/T17–mediated effects on epidermal keratinocytes (KCs) in psoriatic skin. Schematic showing the broad downstream effects of increased IL-23 and IL-17 signaling on various immune cell populations and keratinocyte biology. Regulated by IL-23, the primary effects of IL-17 on keratinocytes include indirect induction of epidermal hyperplasia through IL-19 and IL-36, upregulation of the innate immune response and AMPs (eg, hBD2, S100A7, and LL-37), epidermal recruitment of leukocyte subsets (eg, neutrophils and mDCs) through increased production of keratinocyte-derived chemokines, and transcription of multiple proinflammatory genes (eg, IL-1β, IL-6, and IL-8) that act synergistically with TNF to sustain the inflammatory events in psoriatic skin.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3. Fig 2
IL-17–driven initiation of feed forward inflammation in keratinocytes and induction of psoriatic plaques. A working model of psoriasis showing activation and upregulation of IL-17 in a type 17 resident memory T cell (Trm) in prepsoriatic skin. Increased production of IL-17 results in activation of the IL-17 receptor (IL17R) on viable keratinocytes and a feed forward inflammatory response through activation of IL-17–induced transcription factors (eg, C/EBPβ). This feed forward inflammatory response in keratinocytes is self-amplifying and promotes the development of mature psoriatic plaques through recruitment of pathogenic immune cells, epidermal hyperplasia, and overproduction of IL-17–induced keratinocyte-derived gene products (eg, S100A7/8/9, hBD2, lipocalin-2 [LCN2], and CCL20), which are noticeably increased in the upper layers of the epidermis. A granular layer can be absent in mature psoriasis lesions, leading to retained nuclei in surface corneocytes (ie, parakeratosis). Tem, Effector memory T cell.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2017 American Academy of Allergy, Asthma & Immunology Terms and Conditions