Evidence map›Paper›PMID 26041536›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

CARMA3 Is Critical for the Initiation of Allergic Airway Inflammation.

Benjamin Causton, Ravisankar A Ramadas, Josalyn L Cho, Khristianna Jones, Ana Pardo-Saganta, Jayaraj Rajagopal, Ramnik J Xavier, Benjamin D Medoff

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 24% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Lung Immune Cell Niches and the Discovery of New Cell Subtypes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  2. Review
  3. Article
  4. Article
  5. The role of the CBM complex in allergic inflammation and disease.The Journal of allergy and clinical immunology · 2022
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. CARMA3 Mediates Allergic Lung Inflammation in Response to Alternaria alternata.American journal of respiratory cell and molecular biology · 2018
    Article
  11. Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018
    Article
  12. Review
  13. Review
  14. Article
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Benjamin CaustonDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; Division of Rheumatology, Allergy and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129;
Ravisankar A RamadasMerck Research Laboratories, Boston, MA 02115;
Josalyn L ChoDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; Division of Rheumatology, Allergy and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129;
Khristianna JonesDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; Division of Rheumatology, Allergy and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129;
Ana Pardo-SagantaDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; Center for Regenerative Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114;
Jayaraj RajagopalDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; Center for Regenerative Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114;
Ramnik J XavierCenter for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; and Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114.
Benjamin D MedoffDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114; Division of Rheumatology, Allergy and Immunology, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129; bmedoff@mgh.harvard.edu.
Harvard University · USMerck & Co., Inc., Rahway, NJ, USA (United States) · US

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
TRAINING GRANT IN LUNG CELL &MOLECULAR BIOLOGYT32HL007874 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MEDOFF, BENJAMIN DAVID · 1997 to 2011
$4.1M
Defining the role of Hippo signaling in airway injury repair and remodelingR01HL116756 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI RAJAGOPAL, JAYARAJ · 2013 to 2017
$2.2M
Role of Carma1 in Inflammatory Lung DiseaseR01HL088297 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MEDOFF, BENJAMIN DAVID, XAVIER, RAMNIK J · 2008 to 2011
$1.6M
NHLBI NIH HHS R01 HL088297NHLBI NIH HHS R01 HL116756NHLBI NIH HHS T32 HL007874NHLBI NIH HHS T32 HL07874NIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

Innate immune responses to allergens by airway epithelial cells (AECs) help initiate and propagate the adaptive immune response associated with allergic airway inflammation in asthma. Activation of the transcription factor NF-κB in AECs by allergens or secondary mediators via G protein-coupled receptors (GPCRs) is an important component of this multifaceted inflammatory cascade. Members of the caspase recruitment domain family of proteins display tissue-specific expression and help mediate NF-κB activity in response to numerous stimuli. We have previously shown that caspase recruitment domain-containing membrane-associated guanylate kinase protein (CARMA)3 is specifically expressed in AECs and mediates NF-κB activation in these cells in response to stimulation with the GPCR agonist lysophosphatidic acid. In this study, we demonstrate that reduced levels of CARMA3 in normal human bronchial epithelial cells decreases the production of proasthmatic mediators in response to a panel of asthma-relevant GPCR ligands such as lysophosphatidic acid, adenosine triphosphate, and allergens that activate GPCRs such as Alternaria alternata and house dust mite. We then show that genetically modified mice with CARMA3-deficient AECs have reduced airway eosinophilia and proinflammatory cytokine production in a murine model of allergic airway inflammation. Additionally, we demonstrate that these mice have impaired dendritic cell maturation in the lung and that dendritic cells from mice with CARMA3-deficient AECs have impaired Ag processing. In conclusion, we show that AEC CARMA3 helps mediate allergic airway inflammation, and that CARMA3 is a critical signaling molecule bridging the innate and adaptive immune responses in the lung.

Indexed as

Adaptive ImmunityAdenosine TriphosphateAllergensAlternariaAnimalsAsthmaCARD Signaling Adaptor ProteinsCells, CulturedCytokinesDendritic CellsEpithelial CellsFemaleGene Expression RegulationImmunity, InnateLungLysophospholipidsAdenosine TriphosphateAllergensCard10 protein, mouseCARD Signaling Adaptor ProteinsCytokineslysophosphatidic acidLysophospholipidsNF-kappa BOvalbumin

Identifiers

PMID26041536
PMCPMC4489191
OpenAlexW1511451507

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.