ArticleAmerican journal of physiology. Lung cellular and molecular physiology2006
Contribution of T cell subsets to the pathophysiology of Pneumocystis-related immunorestitution disease.
Article in American journal of physiology. Lung cellular and molecular physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- A machine learning diagnostic model for Pneumocystis jirovecii pneumonia in patients with severe pneumonia.Internal and emergency medicine · 2023Trial
- Immune responses of different hosts toEuropean respiratory review : an official journal of the European Respiratory Society · 2025Review
- T-cell subsets inClinical & translational immunology · 2025Review
- IFN-γ Limits Immunopathogenesis but Delays Fungal Clearance during Pneumocystis Pneumonia.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The Dual Benefit of Sulfasalazine on Pneumocystis Pneumonia-Related Immunopathogenesis and Antifungal Host Defense Does Not Require IL-4Rα-Dependent Macrophage Polarization.Infection and immunity · 2023Article
- Genetic Mouse Models of Pneumocystis Pneumonia.Methods in molecular biology (Clifton, N.J.) · 2023Review
- Supplementary Role of Immunological Indicators in the Diagnosis and Prognosis ofInfection and drug resistance · 2022Article
- Immune Response inJournal of fungi (Basel, Switzerland) · 2021Review
- Combination Immunotherapy with Passive Antibody and Sulfasalazine Accelerates Fungal Clearance and Promotes the Resolution ofInfection and immunity · 2020Article
- Circulating and Pulmonary T-cell Populations Driving the Immune Response in Non-HIV Immunocompromised Patients withInternational journal of medical sciences · 2019Article
- Intrinsic Programming of Alveolar Macrophages for Protective Antifungal Innate Immunity AgainstFrontiers in immunology · 2018Article
- Immune reconstitution inflammatory syndrome associated with pulmonary pathogens.European respiratory review : an official journal of the European Respiratory Society · 2017Review
- Neither classical nor alternative macrophage activation is required for Pneumocystis clearance during immune reconstitution inflammatory syndrome.Infection and immunity · 2015Article
- Innate and Adaptive Cellular Immune Responses to Mycobacterium tuberculosis Infection.Cold Spring Harbor perspectives in medicine · 2015Review
- Pneumocystis.Cold Spring Harbor perspectives in medicine · 2014Review
- MyD88 signaling regulates both host defense and immunopathogenesis during pneumocystis infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Immune reconstitution inflammatory syndrome: the trouble with immunity when you had none.Nature reviews. Microbiology · 2012Review
- Immune Modulation as Adjunctive Therapy for Pneumocystis pneumonia.Interdisciplinary perspectives on infectious diseases · 2011Article
- Immune modulation with sulfasalazine attenuates immunopathogenesis but enhances macrophage-mediated fungal clearance during Pneumocystis pneumonia.PLoS pathogens · 2010Article
- Pneumocystis cell wall beta-glucan stimulates calcium-dependent signaling of IL-8 secretion by human airway epithelial cells.Respiratory research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Immune-mediated lung injury is an important component of Pneumocystis pneumonia (PcP)-related immunorestitution disease (IRD). However, the individual contribution of CD4(+) and CD8(+) T cells to the pathophysiology of IRD remains undetermined. Therefore, IRD was modeled in severe combined immunodeficient mice, and specific T cell depletion was used to determine how T cell subsets interact to affect the nature and severity of disease. CD4(+) cells were more abundant than CD8(+) cells during the acute stage of IRD that coincided with impaired pulmonary physiology and organism clearance. Conversely, CD8(+) cells were more abundant during the resolution phase following P. carinii clearance. Depletion of CD4(+) T cells protected mice from the acute pathophysiology of IRD. However, these mice could not clear the infection and developed severe PcP at later time points when a pathological CD8(+) T cell response was observed. In contrast, mice depleted of CD8(+) T cells efficiently cleared the infection but developed more severe disease, an increased frequency of IFN-gamma-producing CD4(+) cells, and a prolonged CD4(+) T cell response than mice with both CD4(+) and CD8(+) cells. These data suggest that CD4(+) T cells mediate the acute respiratory disease associated with IRD. In contrast, CD8(+) T cells contributed to neither lung injury nor organism clearance when CD4(+) cells were present, but instead served to modulate CD4 function. In the absence of CD4(+) cells, CD8(+) T cells produced a nonprotective, pathological immune response. These data suggest that the interplay of CD4(+) and CD8(+) T cells affects the ultimate outcome of PcP-related IRD.
Indexed as
Identifiers
What OpenQuestion holds
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.