CD93 regulates central nervous system inflammation in two mouse models of autoimmune encephalomyelitis.
Immunology
; 155(3): 346-355, 2018 11.
Article
em En
| MEDLINE
| ID: mdl-29923617
ABSTRACT
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 Lectinhigh Cox2high ). 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.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Medula Espinal
/
Glicoproteínas de Membrana
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Receptores de Complemento
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Regulação da Expressão Gênica
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Microglia
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Encefalomielite Autoimune Experimental
Limite:
Animals
Idioma:
En
Revista:
Immunology
Ano de publicação:
2018
Tipo de documento:
Article
País de afiliação:
Reino Unido