ArticleThe American journal of pathology2010
Type-I IFN signaling suppresses an excessive IFN-gamma response and thus prevents lung damage and chronic inflammation during Pneumocystis (PC) clearance in CD4 T cell-competent mice.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 29 citations in OpenAlex.
- Type I interferons in tuberculosis pathogenesis and prevention.Trends in microbiology · 2026Review
- Unique Immune Polarization of the Lung Allograft: Implications for Organ-specific Immunoregulation and Tolerance Induction.Transplantation · 2026Review
- T-cell subsets inClinical & translational immunology · 2025Review
- Article
- Immunobiology and immunotherapy of COVID-19: A clinically updated overview.Journal of cellular physiology · 2021Review
- Review
- Prevention and treatment of COVID-19: Focus on interferons, chloroquine/hydroxychloroquine, azithromycin, and vaccine.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Circulating and Pulmonary T-cell Populations Driving the Immune Response in Non-HIV Immunocompromised Patients withInternational journal of medical sciences · 2019Article
- Type I Interferon Signaling Is Required for CpG-Oligodesoxynucleotide-Induced Control ofFrontiers in immunology · 2018Article
- Chemokine Receptor Ccr7 Restricts Fatal West Nile Virus Encephalitis.Journal of virology · 2017Article
- OM-85 is an immunomodulator of interferon-β production and inflammasome activity.Scientific reports · 2017Article
- Higher-Order Chromatin Regulation of Inflammatory Gene Expression.Mediators of inflammation · 2017Review
- Article
- Article
- Vascular Dysfunction in Pneumocystis-Associated Pulmonary Hypertension Is Related to Endothelin Response and Adrenomedullin Concentration.The American journal of pathology · 2016Article
- The role of macrophage IL-10/innate IFN interplay during virus-induced asthma.Reviews in medical virology · 2015Review
- Regulation of IFN-γ by IL-13 dictates susceptibility to secondary postinfluenza MRSA pneumonia.European journal of immunology · 2014Article
- Modulation of inflammasome-mediated pulmonary immune activation by type I IFNs protects bone marrow homeostasis during systemic responses to Pneumocystis lung infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- STAT4-dependent and -independent Th2 responses correlate with protective immunity against lung infection with Pneumocystis murina.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Biomimetic antigenic nanoparticles elicit controlled protective immune response to influenza.ACS nano · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Immune-reconstitution after highly active antiretroviral therapy (HAART) is often incomplete, and some HIV-infected individuals fail to regenerate type-I interferon (IFN)-producing pDCs. We recently demonstrated that during Pneumocystis (PC) infection in CD4 T cell-competent mice the absence of type-I IFN signaling results in chronic pulmonary inflammation and fibrosis despite clearance. Because the mechanisms involved are poorly understood, we further characterized the role of type-I IFN signaling in immune responses to PC. We show that type-I IFN signaling around day 7 postinfection is critical to the outcome of inflammation. Microarray analysis of pulmonary CD11c(+) cells revealed that at day 7 post infection, wild-type cells up-regulated type-I IFN-responsive genes as well as SOCS1, which is a critical negative-regulator of type-I IFN and IFN-gamma signaling. This was associated with an eosinophilic lung inflammation, PC clearance, and complete restitution. However, pulmonary CD11c(+) cells from IFNAR(-/-) mice demonstrated increased tumor necrosis factor (TNF)-alpha production and lacked SOCS1-induction at day 7. This was followed by a transient lymphocytic and IFN-gamma response before switching to a chronic eosinophilic inflammation of the lung. Early neutralization of TNF-alpha did not prevent chronic inflammation in IFNAR(-/-) mice, but treatment with an anti-IFN-gamma antibody did. We propose that during PC lung infection type-I IFNs induce SOCS1-associated regulatory mechanisms, which prevent excessive IFN-gamma-mediated responses that cause chronic lung damage. Therefore, partial immune-reconstitution in AIDS, attributable to reduced type-I IFN actions, might disrupt regulatory aspects of inflammation, causing unexplained chronic pulmonary complications as seen in some patients during HAART.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.