Immunopathological inflammation in patients with psoriasis is effectively reduced by bimekizumab treatment targeting simultaneously IL-17A and IL-17F
Abstract
Immunopathological inflammation in psoriasis patients is probably initiated in skin by the presence of damage associated patterns and/or patterns of microbial invasion. These patterns are identified by receptors with subsequent activation of downstream signalling pathways ultimating in transcription of several hundreds proinflammatory genes in innate immunity cells and keratinocytes.
Abnormal functional polarisation of T cells into Th17 subset is mediated by regulatory axis IL-12/IL-23. T cells of Th17 subset, TcRγδ T cells, ILC3 cells and keratinocytes are rich source of IL-17A and IL-17F interleukines which playing the substantial role in immunopathogenesis of psoriasis.
Bimekizumab, monoclonal antibody targeting dualy both IL-17A/IL-17F has demonstrated excellent clinical impact on diseases activity in psoriasis patients.