ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
CD4+ cells are required for chronic eosinophilic lung inflammation but not airway remodeling.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 50 citations in OpenAlex.
- Role for the metalloproteinase ADAM28 in the control of airway inflammation, remodelling and responsiveness in asthma.Frontiers in immunology · 2022Article
- Sialic Acid-Siglec Axis as Molecular Checkpoints Targeting of Immune System: Smart Players in Pathology and Conventional Therapy.International journal of molecular sciences · 2020Review
- Effective lung-targeted RNAi in mice with peptide-based delivery of nucleic acid.Scientific reports · 2019Article
- Similar immune mechanisms control experimental airway eosinophilia elicited by different allergens and treatment protocols.BMC immunology · 2019Article
- T cells and ILC2s are major effector cells in influenza-induced exacerbation of allergic airway inflammation in mice.European journal of immunology · 2019Article
- Synergistic activation of pro-inflammatory type-2 CD8Mucosal immunology · 2018Article
- Induced Regulatory T Cells Superimpose Their Suppressive Capacity with Effector T Cells in Lymph NodesFrontiers in immunology · 2017Article
- Smooth muscle CaMKIIδ promotes allergen-induced airway hyperresponsiveness and inflammation.Pflugers Archiv : European journal of physiology · 2015Article
- Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33.The Journal of allergy and clinical immunology · 2015Article
- At the bench: understanding group 2 innate lymphoid cells in disease.Journal of leukocyte biology · 2015Review
- The immunology of asthma.Nature immunology · 2015Article
- Detection and monitoring of localized matrix metalloproteinase upregulation in a murine model of asthma.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Dietary fish oil and DHA down-regulate antigen-activated CD4+ T-cells while promoting the formation of liquid-ordered mesodomains.The British journal of nutrition · 2014Article
- Lymphocyte-based model systems for allergy research: a historic overview.International archives of allergy and immunology · 2014Review
- Article
- Effects of interleukin-9 blockade on chronic airway inflammation in murine asthma models.Allergy, asthma & immunology research · 2013Article
- The p110δ subunit of PI3K regulates bone marrow-derived eosinophil trafficking and airway eosinophilia in allergen-challenged mice.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Attenuation of antigen-induced airway hyperresponsiveness and inflammation in CXCR3 knockout mice.Respiratory research · 2011Article
- The tumor necrosis factor family member LIGHT is a target for asthmatic airway remodeling.Nature medicine · 2011Article
- Herpesvirus entry mediator (TNFRSF14) regulates the persistence of T helper memory cell populations.The Journal of experimental medicine · 2011Article
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
The contribution of CD4 T cells and other CD4+ cells to lung inflammation and airway remodeling remains unclear during bouts of chronic exposure to airborne allergen. Previously, murine models have shown that CD4 T cells are required for initiation of acute inflammation and the remodeling process. However, it is unknown whether CD4 T cells or other CD4+ cells continue to be required for remodeling during ongoing allergen challenges after the development of acute eosinophilic lung inflammation. To test this, mice were sensitized and challenged with ovalbumin (OVA). After acute airway inflammation was established, a CD4 depleting antibody was administered for 4 wk during a period of chronic exposure to intranasal OVA, resulting in effective depletion of CD4+ cells from all organs, including the lung, lung-draining lymph nodes, and spleen. In these mice, levels of peribronchial inflammation, bronchoalveolar (BAL) eosinophils, and lung CD11c+, CD8+, and Siglec-F+CD11c- cells were significantly reduced. However, mucus metaplasia, peribronchial subepithelial fibrosis, and smooth muscle mass were not affected. Additionally, depletion of CD4+ cells before the last week of chronic allergen challenges also led to significant reductions in BAL eosinophils, peribronchial inflammation, and lung CD11c+, CD8+, and Siglec-F+CD11c- cells. These results show that CD4 T cells, and other CD4+ cells including subsets of dendritic cells, iNKT cells, and LTi cells, play a role in ongoing eosinophilic lung inflammation during periods of chronic allergen challenge, but are not required for progressive airway remodeling that develops after initial acute inflammation.
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.