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. Author manuscript; available in PMC: 2011 Mar 1.
Published in final edited form as: Semin Cutan Med Surg. 2010 Mar;29(1):3–9. doi: 10.1016/j.sder.2010.03.001

Figure 4. NFκB pathway in psoriasis.

Figure 4

Multiple “danger” signals, including TNF, IL-1, toll-like receptor (TLR) ligands and IL-17, may stimulate the transcription factor, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), to translocate into the nucleus and promote the transcription of inflammatory genes. Gene polymorphisms that promote unregulated NFkB activity may contribute to psoriasis susceptibility. Genome-wide associated studies (GWAS) have identified polymorphisms in TNFAIP3 and TNIP1, both negative regulators of the NFκB pathway (box).