The Immunologic Function of the Choroid Plexus: A Gateway to Immunomodulatory Therapy in Injury Models of the Central Nervous System
Authors:
- Roxana Rodriguez-BarreraRRRoxana Rodriguez-Barrera
- Yolanda Cruz-MartínezYCYolanda Cruz-Martínez
- Emilio Moreno-GonzálezEMEmilio Moreno-González
- Elisa GarciaEGElisa Garcia
- Guadalupe Gonzalez-PachecoGGGuadalupe Gonzalez-Pacheco
- Sion Yu JangSJSion Yu Jang
- Adan PeñaAPAdan Peña
- Antonio IbarraAntonio Ibarra
- Rodolfo David Mayen QuintoRQRodolfo David Mayen Quinto
- Iván Ignacio MejíaIMIván Ignacio Mejía
- Exsal Manuel Albores-MéndezEAExsal Manuel Albores-Méndez
- Melchor Castro MarínMMMelchor Castro Marín
Open Access
- 7 July 2026
- journal article
- review article
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (13) , 6074
Abstract
Over time, our understanding of the central nervous system (CNS) as an immunologically privileged site where immune-cell infiltration takes place has changed; research has transformed the dominant view, showing that the CNS is an immunologically specialized tissue featuring complex interactions between the immune system and CNS processes, where the choroid plexus (CP) has an essential role in regulating neuronal tissue homeostasis and immune-cell trafficking. Although immune-cell entry into the CNS is tightly controlled, small numbers of antigen-experienced lymphocytes can access cerebrospinal fluid (CSF) compartments for immune surveillance under normal conditions. During an injury, such as cerebral ischemia or spinal cord damage, dendritic cell precursors infiltrate the CNS, suggesting their involvement in modulating lymphocyte activity. However, the immunoregulatory function of the CP alone is insufficient to prevent damage. Injury can trigger a cascade of events including activation of microglia toward a pro-inflammatory M1 phenotype, infiltration of peripheral immune cells across the blood–brain barrier (BBB), and uncontrolled neuroinflammation. T cells play a critical role in this process. Th1 cells exacerbate inflammation upon recognizing neural antigens, whereas Th2 cells promote recovery by releasing neurotrophic factors. This highlights the dual role of inflammation in CNS injury and repair.Keywords
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