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Transient tear hyperosmolarity disrupts the neuroimmune homeostasis of the ocular surface and facilitates dry eye onset
Author(s) -
Guzmán Mauricio,
Miglio Maximiliano,
Keitelman Irene,
Shiromizu Carolina Maiumi,
Sabbione Florencia,
Fuentes Federico,
Trevani Analía S.,
Giordano Mirta N.,
Galletti Jeremías G.
Publication year - 2020
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13243
Subject(s) - homeostasis , pathogenesis , immunology , medicine , microbiology and biotechnology , biology , pathology , endocrinology
Transient exposure to tear hyperosmolarity without desiccation is sufficient to disrupt the neuroimmune homeostasis of the murine ocular surface. This treatment elicits sub‐clinical dry eye findings, such as increased conjunctival dendritic cell recruitment and maturation, more CD4 + T‐cell activation, and changes in corneal nerve morphology and function. Also, the pathogenic CD4 + T‐cells induced by tear hyperosmolarity promote full dry eye onset in naïve recipients.