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Transient Depletion of CD169⁺ Cells Contributes to Impaired Early Protection and Effector CD8⁺ T Cell Recruitment against Mucosal Respiratory Syncytial Virus Infection.

ABSTRACT: Respiratory syncytial virus (RSV) is a major cause of respiratory viral infections in infants and children. Alveolar macrophages (AMs) play a crucial role in combatting airborne pathogens, strongly express CD169, and are localized in the lung alveoli. Therefore, we used CD169-diphtheria toxin receptor (DTR) transgenic mice to explore the roles of CD169⁺ cells in immune responses to mucosal RSV infection. The administration of diphtheria toxin to CD169-DTR mice induced specific AM depletion and reduced the recruitment of Ly6C^hi monocytes. Notably, CD169⁺ cell depletion reduced levels of innate cytokines, such as interferon-β, IL-6, and TNF-α, in bronchoalveolar lavage fluid during RSV infection without affecting the production of proinflammatory chemokines.

SUBMITTER: Oh DS

PROVIDER: S-EPMC5507946 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Transient Depletion of CD169⁺ Cells Contributes to Impaired Early Protection and Effector CD8⁺ T Cell Recruitment against Mucosal Respiratory Syncytial Virus Infection.

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Dataset Information

Transient Depletion of CD169+ Cells Contributes to Impaired Early Protection and Effector CD8+ T Cell Recruitment against Mucosal Respiratory Syncytial Virus Infection.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Transient Depletion of CD169⁺ Cells Contributes to Impaired Early Protection and Effector CD8⁺ T Cell Recruitment against Mucosal Respiratory Syncytial Virus Infection.