Abstract
Psoriasis is a chronic, inflammatory skin disease, associated with cardiovascular comorbidities, metabolic syndrome, neoplasia, psychiatric impairment and arthritis (among others), which affect patients' quality of life, as well as their life expectancy. Even though it is a multifactorial process of unknown causes, its relationship to class 1 HLA alleles and their polymorphisms has been described. Its physiopathology involves a dysregulation of the systemic inflammatory response, mediated by T Helper lymphocytes, dermal cells, cytokines and interleukins, and their interactions with keratinocytes and sinovial cells. This triggers a differentiation of lymphocytes towards a Th 17 phenotype, which activates inflammatory processes mediated mainly by interleukin 17 (IL-17), with the subsequent proliferation of keratinocytes and inflammatory and angiogenic mediators, resulting in the typical cutaneous and osteoarticular clinical features. Biological agents are recombinat proteins produced in different cell lines aimed at interrupting inflammatory pathways in psoriasis and psoriatic arthritis, specifically, immune or genetic mediators involved in the progression of these diseases, ultimately targeting the IL-23/IL-17 axis. The following article includes the most recent clinical trials regarding the use of biological agents, in particular, IL-23 inhibitors in the treatment of psoriasis and psoriatic arthritis.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Latin american journal of clinical sciences and medical technology
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.