| First Author | Kertser A | Year | 2019 |
| Journal | Sci Adv | Volume | 5 |
| Issue | 5 | Pages | eaav4111 |
| PubMed ID | 31149632 | Mgi Jnum | J:288090 |
| Mgi Id | MGI:6415860 | Doi | 10.1126/sciadv.aav4111 |
| Citation | Kertser A, et al. (2019) Corticosteroid signaling at the brain-immune interface impedes coping with severe psychological stress. Sci Adv 5(5):eaav4111 |
| abstractText | The immune system supports brain plasticity and homeostasis, yet it is prone to changes following psychological stress. Thus, it remains unclear whether and how stress-induced immune alterations contribute to the development of mental pathologies. Here, we show that following severe stress in mice, leukocyte trafficking through the choroid plexus (CP), a compartment that mediates physiological immune-brain communication, is impaired. Blocking glucocorticoid receptor signaling, either systemically or locally through its genetic knockdown at the CP, facilitated the recruitment of Gata3- and Foxp3-expressing T cells to the brain and attenuated post-traumatic behavioral deficits. These findings functionally link post-traumatic stress behavior with elevated stress-related corticosteroid signaling at the brain-immune interface and suggest a novel therapeutic target to attenuate the consequences of severe psychological stress. |
