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<p>Psoriasis is a chronic inflammatory disease affecting approximately 2–3% of the global population, with elevated mortality risk compared to healthy individuals. Currently, over 125&#xa0;million people worldwide are affected, and prevalence continues to rise. The condition is driven by systemic inflammation and is strongly associated with comorbidities, particularly cardiovascular diseases and metabolic syndrome. At the molecular level, psoriasis arises from complex genetic, epigenetic, and environmental interactions, resulting in epidermal hyperplasia and dysregulated keratinocyte differentiation. Despite major therapeutic advances, no definitive cure exists, and disease recurrence following withdrawal of biologics or systemic therapies remains a major clinical challenge. Current treatments primarily target inflammatory pathways and indirectly influence the T<sub>H</sub>17/T<sub>reg</sub> balance, but do not specifically restore regulatory T cell (T<sub>reg</sub>) function or fully correct underlying immune dysregulation. This review focuses on the T<sub>H</sub>17/T<sub>reg</sub> imbalance as a central driver of psoriasis pathogenesis and chronic inflammation, while also discussing its contribution to disease persistence and the multifactorial nature of post-treatment recurrence. Thus, an effort has been made to evaluate cellular, molecular, genetic, and therapeutic perspectives aimed at restoring long-term immune regulation.</p> Graphical abstract

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Immunopathology of psoriasis: a focus on TH17/Treg dynamics & their potential impact on disease recurrence

  • 期刊论文

  • 发表日期：

    2026年5月18日

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  • Rout George Kerry,
  • Asit Ray,
  • Pratap Chandra Panda,
  • Vinayak Nayak,
  • Sushmita Patra,
  • Rakesh Pandey,
  • Bhabani S. Mohanty,
  • Abinash Dutta,
  • Ganesh Kumar Maurya,
  • Jyoti Ranjan Rout,
  • Sanghamitra Nayak

摘要

Psoriasis is a chronic inflammatory disease affecting approximately 2–3% of the global population, with elevated mortality risk compared to healthy individuals. Currently, over 125 million people worldwide are affected, and prevalence continues to rise. The condition is driven by systemic inflammation and is strongly associated with comorbidities, particularly cardiovascular diseases and metabolic syndrome. At the molecular level, psoriasis arises from complex genetic, epigenetic, and environmental interactions, resulting in epidermal hyperplasia and dysregulated keratinocyte differentiation. Despite major therapeutic advances, no definitive cure exists, and disease recurrence following withdrawal of biologics or systemic therapies remains a major clinical challenge. Current treatments primarily target inflammatory pathways and indirectly influence the TH17/Treg balance, but do not specifically restore regulatory T cell (Treg) function or fully correct underlying immune dysregulation. This review focuses on the TH17/Treg imbalance as a central driver of psoriasis pathogenesis and chronic inflammation, while also discussing its contribution to disease persistence and the multifactorial nature of post-treatment recurrence. Thus, an effort has been made to evaluate cellular, molecular, genetic, and therapeutic perspectives aimed at restoring long-term immune regulation.

Graphical abstract