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- W4313365826 abstract "Abstract Barrier immunity, particularly at mucosal surfaces, provides a first line of defense against invading pathogens. Unlike classical mucosal barrier surfaces in the gut and respiratory tract, the olfactory epithelium within the nose is a specialized barrier structure containing layers of olfactory sensory neurons (OSNs) dedicated to our sense of smell. Within nasal airways, OSNs are vulnerable to infection but also directly connected to the brain, thus anatomically, the olfactory epithelium functions as a mucosal barrier to the central nervous system (CNS). Upper respiratory viral infections can damage the olfactory neuroepithelium and are associated with loss of olfaction. Neurotropic viruses, such as vesicular stomatitis virus (VSV), readily infect OSNs, yet the olfactory epithelial response to infection is unknown. VSV infection drove a massive influx of hematopoietic cells including antigen presenting cells and antigen specific CD4+ and CD8+ T cells that established residence within the olfactory epithelium after viral clearance. Upon rechallenge, neutralizing antibody completely protected the neuronal tissues of the olfactory mucosa and the CNS, however this protection appeared to be secretory IgA independent. Resident memory T cells within the olfactory mucosa rapidly produced effector cytokines and prevented heterotypic viral challenge from accessing the CNS. Olfactory VSV infection also resulted in widespread viral and immune mediated tissue damage that contributed to permanent changes in airway turbinate structure. Collectively, these studies offer insight into how the olfactory barrier remodels its neural-immune architecture to provide enhanced protection following a viral challenge." @default.
- W4313365826 created "2023-01-06" @default.
- W4313365826 creator A5069660561 @default.
- W4313365826 date "2019-05-01" @default.
- W4313365826 modified "2023-09-29" @default.
- W4313365826 title "Mucosal immune mediated protection of the CNS following olfactory viral infection" @default.
- W4313365826 doi "https://doi.org/10.4049/jimmunol.202.supp.66.7" @default.
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