Psoriasis Pathogenesis and the Development of Novel, Targeted Immune Therapies
By J. Hawkes, T. Chan, J. Krueger. Journal of Allergy and Clinical Immunology, 2017
867 citations recorded by the source corpus.
&NA; Psoriasis is caused by a complex interplay between the immune system, psoriasis‐associated susceptibility loci, autoantigens, and multiple environmental factors. Over the last 2 decades, research has unequivocally shown that psoriasis represents a bona fide T cell–mediated disease primarily driven by pathogenic T cells that produce high levels of IL‐17 in response to IL‐23. The discovery of the central role for the IL‐23/type 17 T‐cell axis in the development of psoriasis has led to a major paradigm shift in the pathogenic model for this condition. The activation and upregulation of IL‐17 in prepsoriatic skin produces a “feed forward” inflammatory response in keratinocytes that is self‐amplifying and drives the development of mature psoriatic plaques by inducing epidermal hyperplasia, epidermal cell proliferation, and recruitment of leukocyte subsets into the skin. Clinical trial data for mAbs against IL‐17 signaling (secukinumab, ixekizumab, and brodalumab) and newer IL‐23p19 antagonists (tildrakizumab, guselkumab, and risankizumab) underscore the central role of these cytokines as predominant drivers of psoriatic disease. Currently, we are witnessing a translational revolution in the treatment and management of psoriasis. Emerging bispecific antibodies offer the potential for even better disease control, whereas small‐molecule drugs offer future alternatives to the use of biologics and less costly long‐term disease management.
Subfields: Dermatology, Immunology, Physiology
View Paper: https://www.semanticscholar.org/paper/fbb33f85872b1ad9a7fbdeb2dba22d4a65f32d52
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Citations in the corpus
- Structural activation of pro-inflammatory human cytokine IL-23 by cognate IL-23 receptor enables recruitment of the shared receptor IL-12Rβ1 (2017, background): “This is an area that has been extensively developed over the last decade via antibody and non-antibody protein scaffolds alike (Desmet et al., 2014; Hawkes et al., 2017; Ramamurthy et al., 2012).”