Genetics of Psoriasis and Pharmacogenetics of Biological Drugs

Figure 1

Simplified representation of the main mediators of inflammation in psoriasis, the therapeutic targets of biological drugs, and oral alternatives currently under development. Th: helper T lymphocyte; LB: lymphocyte B; APOE: apolipoprotein E; TNF: tumor necrosis factor; IL: interleukin; RANTES, chemokine regulated on activation normal T cells expressed and secreted; CCL: chemokine Cys-Cys motif ligand; MIP: macrophage inflammatory protein; MCP: monocyte chemoattractant protein; PDE4: phosphodiesterase 4; cAMP: cyclic adenosine monophosphate; IFN: interferon; JAK: Janus kinase; STAT: signal transducer and activator of transcription; NF-κBIA: nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor; NF-κB/REL: nuclear factor kappa B/v-rel reticuloendotheliosis viral oncogene complex; a: infliximab, mouse variable region; b: adalimumab, human variable region; c: etanercept, Human TNRFp75 (TNRF2); (−) indicates inhibition and (→) indicates stimulation.