| First Author | Griffiths MR | Year | 2018 |
| Journal | Immunology | Volume | 155 |
| Issue | 3 | Pages | 346-355 |
| PubMed ID | 29923617 | Mgi Jnum | J:266126 |
| Mgi Id | MGI:6202508 | Doi | 10.1111/imm.12974 |
| Citation | Griffiths MR, et al. (2018) CD93 regulates central nervous system inflammation in two mouse models of autoimmune encephalomyelitis. Immunology 155(3):346-355 |
| abstractText | Microglia and non-professional immune cells (endothelial cells, neurons) participate in the recognition and removal of pathogens and tissue debris in the injured central nervous system through major pro-inflammatory processes. However, the mechanisms involved in regulating these responses remain ill-characterized. We herein show that CD93, also known as complement C1qRp/AA4 stem cell marker, has an important role in the regulation of inflammatory processes. The role of CD93 was evaluated in two models of neuroinflammation. We used the MOG-experimental autoimmune encephalomyelitis (EAE) model and the antibody-dependent EAE (ADEAE), which were induced in wild-type and CD93 knockout mice. We found that CD93 was highly expressed by neurons, endothelial cells and microglia (ramified >> amoeboid). Astrocytes and oligodendrocytes did not to express CD93. We further observed that CD93-deficient (CD93(-/-) ) mice presented a more robust brain and spinal cord inflammation in EAE and ADEAE. Encephalitis in CD93(-/-) was characterized by increased numbers of infiltrating M1 macrophages (CD11c(+) CD206(-) ) and amoeboid microglia exhibiting a more activated phenotype (Tomato Lectin(high) Cox2(high) ). Damage to and leakage through the blood-brain barrier was increased in CD93(-/-) animals and was associated with a more robust neuronal injury when compared with wild-type EAE mice. We propose that CD93 is an important neuro-immune regulator to control central nervous system inflammation. |
