Book Description
The innate immune response serves as the body's first line of defense against pathogens and is a critical player in psoriasis development. Genetic variations influencing the components of the innate immune system, such as keratinocytes, dendritic cells, and macrophages, significantly affect disease mechanisms. Keratinocytes in psoriatic lesions express heightened levels of antimicrobial peptides (AMPs) like cathelicidin and β-defensin, which are tightly regulated by genetic factors. Increased AMP expression can perpetuate inflammation by acting as chemoattractants for immune cells and by triggering pro-inflammatory cytokine production. Moreover, single nucleotide polymorphisms (SNPs) in genes coding for innate immune receptors, such as Toll-like receptors (TLRs), have been associated with increased susceptibility to psoriasis. For instance, genetic variants affecting TLR signaling can lead to an exaggerated inflammatory response to environmental triggers, such as trauma or infections, commonly associated with psoriasis flares. This implicates TLR-mediated pathways as crucial targets for therapeutic intervention, as modulation of this signaling can alter disease progression.
