Skip to main content
. 2019 Oct 7;20:546–553. doi: 10.1016/j.isci.2019.10.008

Figure 2.

Figure 2

Modeling Plaque Formation in Psoriasis

(A) Interactions between key cytokines involved in psoriasis plaque formation. Labels numbered 0–4 refer to the observations from which these interactions have been inferred (see Results).

(B) A simplified diagram of interactions, in which cytokines IL-17 and TNF-α are considered jointly.

(C) Diagram (B) relabeled as an activator (A) - depleted substrate (S) system.

(D) Skin representation and simulation initialization. The skin surface is partitioned into square regions. A lesion is initiated by an activated TH17 cell (red), which is either a resident memory T cell activated by a dendritic cell (green, interaction a) or has migrated from circulation through a capillary wall (interaction b). The area of microinflammation around the activated TH17 cell is considered as a “seed” region, and its projection to the surface (arrow c) is colored in red. The epidermis, the upper layer of the skin, is shaded in gray and capillaries in the dermis are colored in red (arterioles) and blue (venules). Skin-resident memory T cells are marked in gray.

(E) Detail of skin surface representation. Each region is a two-dimensional projection of the underlying activator-depleted substrate system of proinflammatory cytokines and represents a computational cell implementing reaction system (C). These computational cells are interconnected (double arrows), allowing for the diffusion of cytokines.