ArticleInternational journal of medical sciences2009
Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta.
Article in International journal of medical sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Pro-lymphangiogenic VEGFR-3 signaling modulates memory T cell responses in allergic airway inflammation.Mucosal immunology · 2021Article
- Intestinal transcriptional profiling reveals fava bean-induced immune response in DBA/1 mice.Biological research · 2019Article
- Abr, a negative regulator of Rac, attenuates cockroach allergen-induced asthma in a mouse model.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Role of Chemokines and Trafficking of Immune Cells in Parasitic Infections.Current immunology reviews · 2013Article
- CNS-derived CCL21 is both sufficient to drive homeostatic CD4+ T cell proliferation and necessary for efficient CD4+ T cell migration into the CNS parenchyma following Toxoplasma gondii infection.Brain, behavior, and immunity · 2011Article
- CCR7-dependent immunity during acute Toxoplasma gondii infection.Infection and immunity · 2010Article
- Article
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The chemokines CCL21 and CCL19, and cell bound TNF family ligand lymphotoxin beta (LTbeta), have been associated with numerous chronic inflammatory diseases. A general role in chronic inflammatory diseases cannot be assumed however; in the case of allergic inflammatory disease, CCL21/CCL19 and LTbeta have not been associated with the induction, recruitment, or effector function of Th2 cells nor dendritic cells to the lung. We have examined the induction of allergic inflammatory lung disease in mice deficient in CCL21/CCL19 or LTbeta and found that both kinds of mice can develop allergic lung inflammation. To control for effects of priming differences in knockout mice, adoptive transfers of Th2 cells were also performed, and they showed that such effector cells had equivalent effects on airway hyper-responsiveness in both knockout background recipients. Moreover, class II positive antigen presenting cells (B cells and CD11c+ dendritic cells) showed normal recruitment to the peribronchial spaces along with CD4 T cells. Thus, the induction of allergic responses and recruitment of both effector Th2 cells and antigen presenting cells to lung peribronchial spaces can develop independently of CCL21/CCL19 and LTbeta.
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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.