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Cell Host Microbe. 2009 Nov 19;6(5):470-81. doi: 10.1016/j.chom.2009.10.007.

Inflammatory monocytes facilitate adaptive CD4 T cell responses during respiratory fungal infection.

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1
Infectious Disease Service, Department of Medicine, and Immunology Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA. thohl@fhcrc.org

Abstract

Aspergillus fumigatus, a ubiquitous fungus, causes invasive disease in immunocompromised humans. Although monocytes and antigen-specific CD4 T cells contribute to defense against inhaled fungal spores, how these cells interact during infection remains undefined. Investigating the role of inflammatory monocytes and monocyte-derived dendritic cells during fungal infection, we find that A. fumigatus infection induces an influx of chemokine receptor CCR2- and Ly6C-expressing inflammatory monocytes into lungs and draining lymph nodes. Depletion of CCR2(+) cells reduced A. fumigatus conidial transport from lungs to draining lymph nodes, abolished CD4 T cell priming following respiratory challenge, and impaired pulmonary fungal clearance. In contrast, depletion of CCR2(+)Ly6C(hi) monocytes during systemic fungal infection did not prevent CD4 T cell priming in the spleen. Our findings demonstrate that pulmonary CD4 T cell responses to inhaled spores require CCR2(+)Ly6C(hi) monocytes and their derivatives, revealing a compartmentally restricted function for these cells in adaptive respiratory immune responses.

PMID:
19917501
PMCID:
PMC2785497
DOI:
10.1016/j.chom.2009.10.007
[Indexed for MEDLINE]
Free PMC Article

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