Table 2.

Main articles included in the summary of signaling cascades shown in Figure 2.

Article	Main findings
Marble et al. J Dermatol Sci. 2007; 48(2):87-101. [26]	CD11c + dendritic cells, CD68+ macrophages and TNF-α + cells are increased in psoriatic lesions
Ten Bergen et al. Scand J Immunol. 2020; 92(4):e12946. [27]	TNF-α/IL-23/IL-17 axis appears to has central role in the pathophysiology of psoriasis
Bos et al. Br J Dermatol. 2005; 152(6):1098-107. [28]	Activation of innate immunity, represented by the activity of NKT cells, dendritic cells, neutrophils, and keratinocytes, is crucial in pathogenesis of psoriasis.
Chiang et al. Front Immunol. 2019; 10 : 2376. [29]	The abundant presence of neutrophils in the psoriatic skin lesions and formation of Munro's microabscesses serves as a typical histopathologic hallmark of psoriasis.
Kim and Krueger. Dermatol Clin. 2015; 33(1):13-23. [13]	Keratinocytes appear to be important regulators of immune responses, involved in increased production of TNF-α or IFN-γ in psoriasis.
Hawkes et al. J Immunol. 2018; 201(6):1605-1613. [34]	Psoriasis is characterized by the presence of multiple T lymphocyte subsets (Th1, Th17, and Th22).
Stephen-Victor et al. PLoS Pathog. 2016; 12(6):e1005624 [37] Wang et al. J Cell Mol Med. 2019; 23(12):7926-7932. [38]	Th17 cells, besides IL-17, produce TNF-α, IL-26, and IL-29, which further stimulate release of proinflammatory mediators.
Levin and Gottlieb. J Am Acad Dermatol. 2014; 70(3):555-61. [46] Langrish et al. Immunol Rev. 2004; 202 : 96-105. [47]	IL-23 is recognized as a key regulator in psoriasis due to specific role in cross bridging the production of IL-17 by innate and acquired immunity.