Species

Evidence

Reference

Mouse

Overexpression of mRNA transcript levels of IL-17A, IL-17F, IL-23p19, and IL-12/IL-23p40 results in inflammatory skin disease

^19,23,24,27[19, 23, 24, 27]

Injection of IL-17 induced high neutrophilic infiltration in dermis

[17]¹⁷

Increased number of Th17 (CD4+IL-17+) cells in psoriatic lesions

[23]²³

Experimentally induced psoriatic lesions abolished by anti-IL-12/23p40 or anti-IL-23p19 antibodies

^19,23,26[19, 23, 26]

IL-23 or the IL-17 receptor deficiency blocked  inflammatory disease progression

[27]²⁷

Human

IL-23p19 mRNA and protein is increased in psoriatic lesions

[30, 106, 107]^{30,114106,115107}

Increased number of circulating Th17 (CD4+IL-17+) cells and Tc17 (CD8+IL-17+) in psoriatic patients

[34, 40, 41]^34,40,41

Increased mRNA and protein expression of IL-17 in psoriatic lesions

^{30,36-38,11630,36-38,108}[30, 36-38, 108]

Levels of IL-17 correlate with PASI scores and decreased after psoriasis therapy

[35, 39, 95, 96, 98-101, 103]^{35, 39, 103, 104, 106-109, 11195,96,98-101,103}

Increased mRNA expression and protein levels of IL-17-induced effector molecules (antimicrobial peptides, cytokines, and neutrophil-attracting CXCL chemokines) in psoriatic lesions

[44, 51, 52, 109, 110]^{44,51,52,117,118109,110}

A genetic polymorphism in IL-12/IL-23 p40 is linked to increased susceptibility in psoriasis

[53, 54, 56]53,54,5657,58,60

A genetic polymorphism in ACT1 is linked to increased susceptibility in psoriasis

[63]636763