TITLE:
Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Immunopathogenic Basis of Epithelial Collapse and Ocular Damage
AUTHORS:
Gustavo Alberto Gutiérrez-Barros, María Victoria Morales-Morales, Gabriela María Morales-Donado, Sharon Nicole Rueda-Cogollo, María Camila Pardo-Pérez, Juan Camilo Rodríguez-Gale, Isabella María Mercado-Athias, Isabella Pizarro-Castillo, Juan Manuel Gómez-Briñez, Juan Diego Quiroga-Campo, Ángelo Vitola-Lora, Karina Badran-Zapata, Antonio Joaquín Pumarejo-Insignares, Carlos Andrés Morales-Padilla, María José Rojas-Hernández, Eliannys Paola Quintero-Gámez, Edilma Rosa Quintero-Gámez, Ricardo José Boneth-Pérez, Edwin Javier Delgado-Caliz, Sergio Andrés Vides-Ricaurte, María Camila Martínez-Morales, Laurent María Redondo-Athias
KEYWORDS:
Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, Epithelial Necrosis
JOURNAL NAME:
Journal of Biosciences and Medicines,
Vol.14 No.3,
March
24,
2026
ABSTRACT: The spectrum comprising Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) represent a critical model of systemic epithelial disruption, characterized by massive keratinocyte apoptosis mediated by dysregulation of adaptive immunity. Although dermoepidermal denudation defines disease severity during the acute phase, the ocular surface exhibits a distinctive immunopathological susceptibility whose progression toward chronicity may occur independently of the extent of cutaneous injury. This biological autonomy is related to the breakdown of ocular immune privilege and to the intrinsic vulnerability of high-turnover epithelial tissues to targeted cytotoxic aggression. This review describes the pathological pathways that mediate the synchronized destruction of the mucosal barrier, emphasizing the relationship between the immunological mechanisms responsible for epidermal necrosis and the involvement of ocular tissues. The transition from acute denudate keratoconjunctivitis to the progressive collapse of the limbal stem cell niche is examined, evaluating how persistent immune-mediated cytotoxicity, aberrant remodeling of the extracellular matrix, and loss of tissue plasticity promote the development of persistent epithelial defects, conjunctival scarring, and permanent homeostatic failure of the ocular surface.