Doublecortin expression in CD8+ T-cells and microglia at sites of amyloid-β plaques: A potential role in shaping plaque pathology?
| Main Authors: | Unger, Michael S, Marschallinger, Julia, Kaindl, Julia, Klein, Barbara, Johnson, Mary, Khundakar, Ahmad A, Roßner, Steffen, Heneka, Michael T, Couillard-Depres, Sebastien, Rockenstein, Edward, Masliah, Eliezer,, Attems, Johannes, Aigner, Ludwig |
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| Format: | Article Journal |
| Bahasa: | eng |
| Terbitan: |
, 2018
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| Subjects: | |
| Online Access: |
https://zenodo.org/record/1298612 |
Daftar Isi:
- Abstract INTRODUCTION: One characteristic of Alzheimer's disease is the formation of amyloid-β plaques, which are typically linked to neuroinflammation and surrounded by inflammatory cells such as microglia and infiltrating immune cells. METHODS: Here, we describe nonneurogenic doublecortin (DCX) positive cells, DCX being generally used as a marker for young immature neurons, at sites of amyloid-β plaques in various transgenic amyloid mouse models and in human brains with plaque pathology. RESULTS: The plaque-associated DCX+ cells were not of neurogenic identity, instead most of them showed coexpression with markers for microglia (ionized calcium-binding adapter molecule 1) and for phagocytosis (CD68 and TREM2). Another subpopulation of plaque-associated DCX+ cells was negative for ionized calcium-binding adapter molecule 1 but was highly positive for the pan-leukocyte marker CD45. These hematopoietic cells were identified as CD3-and CD8-positive and CD4-negative T-cells. DISCUSSION: Peculiarly, the DCX+/ionized calcium-binding adapter molecule 1+ microglia and DCX+/CD8+ T-cells were closely attached, suggesting that these two cell types are tightly interacting and that this interaction might shape plaque pathology.