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Age-related increases in PGD2 expression impair respiratory DC migration, resulting in diminished T cell responses upon respiratory virus infection in mice
Open accessAbstract
The morbidity and mortality associated with respiratory virus infection is felt most keenly among the elderly. T cells are necessary for viral clearance, and many age-dependent intrinsic T cell defects have been documented. However, the development of robust T cell responses in the lung also requires respiratory DCs (rDCs), which must process antigen and migrate to draining LNs (DLNs), and little is known about age-related defects in these T cell-extrinsic functions. Here, we show that increases in prostaglandin D(2) (PGD(2)) expression in mouse lungs upon aging correlate with a progressive impairment in rDC migration to DLNs. Decreased rDC migration resulted in diminished T cell responses and more severe clinical disease in older mice infected with respiratory viruses. Diminished rDC migration associated with virus-specific defects in T cell responses and was not a result of cell-intrinsic defect, rather it reflected the observed age-dependent increases in PGD(2) expression. Blocking PGD(2) function with small-molecule antagonists enhanced rDC migration, T cell responses, and survival. This effect correlated with upregulation on rDCs of CCR7, a chemokine receptor involved in DC chemotaxis. Our results suggest that inhibiting PGD(2) function may be a useful approach to enhance T cell responses against respiratory viruses in older humans.
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“Age-related elevations of eicosanoid levels, especially prostaglandin D2 (PGD2), were detected in mouse models of SARS-CoV infection133.”
From COVID-19 and cellular senescence (2023) · cites this paper as [133]
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“During SARS-CoV-1 infection, lung DCs from older mice displayed an impaired ability to migrate to the draining lymph node, which negatively affected subsequent T cell priming125.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [125]
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Metadata
- Authors
- Zhao, J., Zhao, J., Legge, K., & Perlman, S.
- Affiliations
- University of Iowa (US)
- Corresponding author
- Perlman, Stanley
- Venue
- Journal of Clinical Investigation
- Published
- 2011-12-01
- Volume
- 121
- Issue
- 12
- Pages
- 4921-4930
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3226008
- OpenAlex
- W2115101593
- Cited by
- 265
- References
- 60
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 8 · 2023: 15 · 2022: 26 · 2021: 42 · 2020: 66 · 2019: 5 · 2018: 10 · 2017: 12 · 2016: 14 · 2015: 9 · 2014: 15 · 2013: 16 · 2012: 6
- FWCI
- 5.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (PO1AI060699, AI060699, AI071085)
- National Institute of Allergy and Infectious Diseases (R01AI071085, R56 AI79424, R01AI091322, R56AI079424, P01AI060699)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Keywords
- prostaglandin D2, dendritic cell migration, aging, respiratory viral infections, T cell response, draining lymph nodes, CCR7, chemokine receptors, age-related immunosenescence, lung immunity
- MeSH terms
- Aging, Animals, Cell Movement, Dendritic Cells, Disease Susceptibility, Murine hepatitis virus, Lung, Lymph Nodes, Lymphocyte Activation, Mice, Inbred C57BL, Orthomyxoviridae Infections, Influenza A virus, Prostaglandin Antagonists, Respiratory Syncytial Viruses, Specific Pathogen-Free Organisms, Prostaglandin D2, T-Lymphocyte Subsets, Immunocompromised Host, Coronavirus Infections, Respiratory Syncytial Virus Infections, Severe Acute Respiratory Syndrome, Severe acute respiratory syndrome-related coronavirus, Mice, Receptors, CCR7, Cellular Microenvironment
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