Advances in Monoclonal Antibody Therapy for Moderate to Severe Psoriasis: Targeting TNF, IL-17, And IL-23 Pathways for Optimal Disease Management

Main Article Content

José Anthar Ávalos Narváez
Kevin Daniel Solís Dittrich
María Elisa González Robles
Michelle Jiménez Zaragoza
Ricardo Arturo Ovilla Alvarez
Mayra Aréchiga López

Abstract

Psoriasis, a chronic immune-mediated dermatological disorder, significantly impacts patients' quality of life, particularly in its moderate to severe forms. The advent of biologic therapies, specifically monoclonal antibodies (mAbs), has revolutionized the treatment landscape. This article provides an in-depth analysis of the efficacy, safety, and mechanistic insights of anti-TNF (e.g., adalimumab, infliximab), anti-IL-17 (e.g., secukinumab, ixekizumab), and anti-IL-23 (e.g., guselkumab, risankizumab) agents in the management of moderate to severe psoriasis. Clinical trials and real-world evidence demonstrate that these biologics achieve substantial improvements in Psoriasis Area and Severity Index (PASI) scores, Dermatology Life Quality Index (DLQI), and long-term remission rates. However, their use is not without risks, including potential adverse effects such as infections, immunogenicity, and rare paradoxical reactions. This review underscores the importance of personalized treatment strategies, considering patient-specific factors such as comorbidities, disease severity, and treatment history. By synthesizing current evidence, this article aims to guide clinicians in optimizing therapeutic outcomes while mitigating risks associated with monoclonal antibody therapy in psoriasis management.

Article Details

How to Cite
José Anthar Ávalos Narváez, Kevin Daniel Solís Dittrich, María Elisa González Robles, Michelle Jiménez Zaragoza, Ricardo Arturo Ovilla Alvarez, & Mayra Aréchiga López. (2025). Advances in Monoclonal Antibody Therapy for Moderate to Severe Psoriasis: Targeting TNF, IL-17, And IL-23 Pathways for Optimal Disease Management. International Journal of Medical Science and Clinical Research Studies, 5(5), 766–769. https://doi.org/10.47191/ijmscrs/v5-i05-17
Section
Articles

References

I. Parisi R, Symmons DP, Griffiths CE, Ashcroft DM. Global epidemiology of psoriasis: a systematic review of incidence and prevalence. JInvestDermatol. (2013) 133:377–85.

doi: 10.1038/jid.2012.339

II. Chiricozzi A, Saraceno R, Chimenti MS, Guttman-Yassky E, Krueger JG. Role of IL-23 in the pathogenesis of psoriasis: a novel potential therapeutic target? Expert Opin Ther Targets. (2014) 18:513–25. doi: 10.1517/14728222.2014.889686

III. Martin DA, Towne JE, Kricorian G, Klekotka P, Gudjonsson JE, Krueger JG, et al. The emerging role of IL-17 in the pathogenesis of psoriasis: preclinical and clinical findings. J Invest Dermatol. (2013) 133:17– 26. doi: 10.1038/jid.2012.194

IV. Bergboer JGM, Zeeuwen P, Schalkwijk J. Genetics of psoriasis: evidence for epistatic interaction between skin barrier abnormalities and immune deviation. JInvestDermatol.(2012) 132:2320–31. doi: 10.1038/jid.2012.167

V. Lupardus PJ, Garcia KC. The structure of interleukin-23 reveals the molecular basis of p40 subunit sharing with interleukin-12.

JMolBiol.(2008) 382:931–41.

doi: 10.1016/j.jmb.2008.07.051

VI. Oppmann B, Lesley R, Blom B, Timans JC, Xu Y, Hunte B, et al. Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity. (2000) 13:715– 25.

doi: 10.1016/S1074-7613(00)00070-4

VII. Di Meglio P, Nestle FO. The role of IL-23 in the immunopathogenesis of psoriasis.

F1000BiolRep.(2010) 2:40. doi: 10.3410/B2-40

VIII. Tang C, Chen S, Qian H, Huang W. Interleukin-23: as a drug target for autoimmune inflammatory diseases. Immunology. (2012) 135:112–24.

doi: 10.1111/j.1365-2567.2011.03522.x

IX. Piskin G, Sylva-Steenland RM, Bos JD, Teunissen MB. In vitro and in situ expression of IL-23 by keratinocytes in healthy skin and psoriasis lesions: enhanced expression in psoriatic skin. J Immunol.(2006) 176:1908–15.

doi: 10.4049/jimmunol.176.3.1908

X. Smits HH, van Beelen AJ, Hessle C, Westland R, de Jong E, Soeteman E, et al. Commensal gram-negative bacteria prime human dendritic cells for enhanced IL-23 and IL-27 expression and enhanced Th1 development. EurJ Immunol.(2004) 34:1371–80. doi: 10.1002/eji.200324815

XI. Liu W, Ouyang X, Yang J, Liu J, Li Q, Gu Y, et al. AP-1 activated by toll-like receptors regulates expression of IL-23 p19. J Biol Chem. (2009) 284:24006–16. doi: 10.1074/jbc.M109.025528

XII. Wilson NJ, Boniface K, Chan JR, McKenzie BS, Blumenschein WM, Mattson JD, et al. Development, cytokine profile and function of human interleukin 17-producing helper T cells. Nat Immunol. (2007) 8:950–7. doi: 10.1038/ni149

Most read articles by the same author(s)