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- Title
Group 2 innate lymphoid cells are numerically and functionally deficient in the triple transgenic mouse model of Alzheimer's disease.
- Authors
Fung, Ivan Ting Hin; Zhang, Yuanyue; Shin, Damian S.; Sankar, Poornima; Sun, Xiangwan; D'Souza, Shanti S.; Song, Renjie; Kuentzel, Marcy L.; Chittur, Sridar V.; Zuloaga, Kristen L.; Yang, Qi
- Abstract
<bold>Background: </bold>The immune pathways in Alzheimer's disease (AD) remain incompletely understood. Our recent study indicates that tissue-resident group 2 innate lymphoid cells (ILC2) accumulate in the brain barriers of aged mice and that their activation alleviates aging-associated cognitive decline. The regulation and function of ILC2 in AD, however, remain unknown.<bold>Methods: </bold>In this study, we examined the numbers and functional capability of ILC2 from the triple transgenic AD mice (3xTg-AD) and control wild-type mice. We investigated the effects of treatment with IL-5, a cytokine produced by ILC2, on the cognitive function of 3xTg-AD mice.<bold>Results: </bold>We demonstrate that brain-associated ILC2 are numerically and functionally defective in the triple transgenic AD mouse model (3xTg-AD). The numbers of brain-associated ILC2 were greatly reduced in 7-month-old 3xTg-AD mice of both sexes, compared to those in age- and sex-matched control wild-type mice. The remaining ILC2 in 3xTg-AD mice failed to efficiently produce the type 2 cytokine IL-5 but gained the capability to express a number of proinflammatory genes. Administration of IL-5, a cytokine produced by ILC2, transiently improved spatial recognition and learning in 3xTg-AD mice.<bold>Conclusion: </bold>Our results collectively indicate that numerical and functional deficiency of ILC2 might contribute to the cognitive impairment of 3xTg-AD mice.
- Subjects
INNATE lymphoid cells; LABORATORY mice; TRANSGENIC mice; ALZHEIMER'S disease; COGNITIVE ability; CELL culture; ANIMAL experimentation; LYMPHOCYTES; IMMUNITY; MICE
- Publication
Journal of Neuroinflammation, 2021, Vol 18, Issue 1, p1
- ISSN
1742-2094
- Publication type
journal article
- DOI
10.1186/s12974-021-02202-2