Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 30% 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
4 citing papers in PubMed, 10 citations in OpenAlex.
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
10 authors at 4 institutions in 3 countries.
Jessica Elmore *Department of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.
Chavez Carter *Department of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.
Amie RedkoDepartment of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.
Nicholas KoylassDepartment of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.
Amelia BennettDepartment of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.
Max MeadDepartment of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.ORCID http://orcid.org/0000-0003-2752-2450
Marinel Ocasio-RiveraDepartment of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.ORCID http://orcid.org/0000-0002-2420-146X
Weishan HuangDepartment of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA.
Ankur SinghNancy E & Peter C Meinig School of Biomedical Engineering and Department of Mechanical & Aerospace Engineering, Cornell University, Ithaca, NY, USA.ORCID http://orcid.org/0000-0002-3501-2277
Avery AugustDepartment of Microbiology & Immunology, Cornell Center for Immunology, Cornell Institute for Host Microbe-Interactions and Disease, Cornell University, Ithaca, NY, USA. averyaugust@cornell.edu.ORCID http://orcid.org/0000-0003-4968-3415
Cornell University · USJohns Hopkins University · USLouisiana State University · USUniversity of Puerto Rico at Río Piedras · PR
Funding
Small RNA Pathways in Mammalian GametogenesisP50HD076210 · NICHD · CORNELL UNIVERSITY · PI COHEN, PAULA ELAINE · 2014 to 2018
$7.4M
UNIVERSITY OF PUERTO RICO PONCE RESEARCH INITIATIVE FOR SCIENTIFIC ENHANCEMENT: UR25GM096955 · NIGMS · UNIVERSITY OF PUERTO RICO PONCE · PI SUAREZ-MARTINEZ, EDU B · 2011 to 2020
$5.7M
Regulation of IL10 production in CD8+ T cells during Flu infection by tyrosine kinase ItkR01AI138570 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY · 2018 to 2022
$2.1M
Biomaterials-based Germinal Center Niches for Understanding the B Cell Maturation and B cell receptor signalingR01AI132738 · NIAID · GEORGIA INSTITUTE OF TECHNOLOGY · PI SINGH, ANKUR · 2018 to 2022
$1.9M
Itk mediated tuning of CD8+ memory T cell developmentR01AI120701 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY · 2016 to 2019
$1.5M
Immuno-Engineering: Integrated Engineering and Immunology TrainingT32EB023860 · NIBIB · CORNELL UNIVERSITY · PI AUGUST, AVERY, PUTNAM, DAVID A · 2018 to 2022
$933k
Itk signaling and Type 1 regulatory T cell differentiation and function in allergic airway inflammationR21AI129422 · NIAID · CORNELL UNIVERSITY · PI AUGUST, AVERY, HUANG, WEISHAN · 2018 to 2019
$431k
Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) AI129422Howard Hughes Medical InstituteNIAID NIH HHS R01 AI120701NIAID NIH HHS R01 AI132738NIAID NIH HHS R01 AI138570NIAID NIH HHS R21 AI129422NIBIB NIH HHS T32 EB023860NICHD NIH HHS P50 HD076210NIGMS NIH HHS R25 GM096955U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI120701U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI129422U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI132738U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI138570
6 · The paper itself
Abstract
T helper 17 (Th17) cells develop in response to T cell receptor signals (TCR) in the presence of specific environments, and produce the inflammatory cytokine IL17A. These cells have been implicated in a number of inflammatory diseases and represent a potential target for ameliorating such diseases. The kinase ITK, a critical regulator of TCR signals, has been shown to be required for the development of Th17 cells. However, we show here that lung inflammation induced by Saccharopolyspora rectivirgula (SR) induced Hypersensitivity pneumonitis (SR-HP) results in a neutrophil independent, and ITK independent Th17 responses, although ITK signals are required for γδ T cell production of IL17A. Transcriptomic analysis of resultant ITK independent Th17 cells suggest that the SR-HP-induced extrinsic inflammatory signals may override intrinsic T cell signals downstream of ITK to rescue Th17 responses in the absence of ITK. These findings suggest that the ability to pharmaceutically target ITK to suppress Th17 responses may be dependent on the type of inflammation.
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 Socratic graph.
ITK independent development of Th17 responses during hypersensitivity pneumonitis driven lung inflammation. · full record | Socratic