“…Thus the SCID model has proved to be a very effective model to explore the role of neurogenic inflammation in psoriasis and has opened a door to the development of drugs targeting the NGF/NGF-R system. [73,74,[81][82][83] In psoriasis there is increased expression of endothelial cell adhesion molecules (E-selectin, ICAM, VCAM), [84][85][86][87] angiogenesis with upregulation of endothelial cell-stimulating angiogenesis factor (ESAF) and VEGF [88,89] activated T-cells (CD4, CD8, NK cells) infiltrates [90][91][92][93] neutrophils (Munro's and Kogoji microabscess), mast cells, [93,94] upregulation of chemokines such as IL-8, RANTES, fractalkine, [17,[95][96][97] and neuropeptides. [71,72,98,99] Likewise, the transplanted psoriatic plaques in SCID mice, demonstrate upregulation of molecules like p38 MAPK, STAT3, ICAM, CXCR3, fractalkine, IL-8, CD3, CD4, CD8, CD40, CD80, CD86, HLA-DR, OX-40R, K16, Ki67, SP, NGF, and NGF-R. Upregulation of CD80/CD86 supports the role of CD28/B7 co-stimulatory cascades in psoriatic inflammation.…”