Evidence map›Paper›PMID 23325004›Full record

ArticleTransplantation2013

Critical role for IL-17A/F in the immunopathogenesis of obliterative airway disease induced by Anti-MHC I antibodies.

Haseeb Ilias Basha, Sabarinathan Ramachandran, Venkataswarup Tiriveedhi, Masashi Takenaka, Vijay Subramanian, Dilip S Nath, Nicholas Benshoff, G Alec Patterson, Thalachallour Mohanakumar

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Transplantation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. HLA and lung transplantation.Frontiers of medicine · 2019
    Review
  4. IL-17 in the lung: the good, the bad, and the ugly.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  5. Article
  6. Review
  7. Environmental Exposures-The Missing Link in Immune Responses After Transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016
    Review
  8. Article
  9. Article
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

9 authors at 1 institution in 1 country.

Haseeb Ilias BashaDepartment of Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA.
Sabarinathan Ramachandran
Venkataswarup Tiriveedhi
Masashi Takenaka
Vijay Subramanian
Dilip S Nath
Nicholas Benshoff
G Alec Patterson
Thalachallour Mohanakumar
Washington University in St. Louis · US

Funding

BASIC SCIENCE RESEARCH TRAINING: CARDIOPULMONARY SURGERYT32HL007776 · NHLBI · WASHINGTON UNIVERSITY · PI DAMIANO, RALPH J · 1994 to 2020
$4.6M
ALLOANTIBODIES TO MHC INDUCES AUTOIMMUNITY AND OBLITERATIVE AIRWAY DISEASE (OAD)R01HL092514 · NHLBI · WASHINGTON UNIVERSITY · PI MOHANAKUMAR, THALACHALLOUR · 2009 to 2018
$3.0M
NHLBI NIH HHS HL092514NHLBI NIH HHS R01 HL092514NHLBI NIH HHS T32 HL007776NHLBI NIH HHS T32 HL07776
6 · The paper itself

Abstract

backgroundThe IL-17 axis is implicated in pathogenesis of chronic rejection after human lung transplantation. Using a murine model of obliterative airway disease (OAD), we recently demonstrated that Abs to MHC class I antigens can induce immune responses to self-antigens that contributes to immunopathogenesis of chronic rejection. Using a murine model of OAD, we determined the role of IL-17 family members in induction of autoimmunity leading to OAD after ligation of MHC class I.

methodsAnti-MHC class I or control antibodies (Abs) were administered intrabronchially to wild-type (WT) and IL-17a knock out (IL-17A-/-) C57BL/6.

resultsBy day 30, anti-MHC I administered endobronchially in IL-17A-/- mice demonstrated significant reduction in cellular infiltration, a 36.8% reduction in CD4 T cells, 62.7% in CD11b macrophages, 37.5% in degree of fibrosis, 1.94 fold and 2.17 fold decrease in anti-KAT and anti-Col-V, respectively, when compared with wild-type mice. Analysis of lung infiltrating cells in anti-MHC I WT revealed increase in IL-17A (KAT:92+21,Col-V:103+19spm) and IL-17F (KAT:5.03%,Col-V:2.75%) secreting CD4+ T cells. However, administration of anti-MHC I in IL-17A-/- demonstrated increase only in IL-17F for KAT (13.70%) and Col-V (7.08%). Anti-IL-17(A-F) mAb administration after anti-MHC I abrogated OAD in both WT and IL-17A-/-.

conclusionOur findings indicate that IL-17A and IL-17F secreted by CD4+Th17 cells specific to lung self-antigens are critical mediators of autoimmunity leading to the pathogenesis of OAD.

Indexed as

AutoimmunityAnimalsAntibodies, MonoclonalAntibodies, NeutralizingAutoantibodiesBiomarkersBronchiolesBronchiolitis ObliteransCD11b AntigenCollagen Type VDisease Models, AnimalForkhead Transcription FactorsHistocompatibility Antigens Class IInflammation MediatorsInterleukin-17Interleukin-2 Receptor alpha SubunitAntibodies, MonoclonalAntibodies, NeutralizingAutoantibodiesBiomarkersCD11b AntigenCollagen Type VForkhead Transcription FactorsFoxp3 protein, mouseHistocompatibility Antigens Class IIl17a protein, mouseIl17f protein, mouseIl2ra protein, mouseInflammation MediatorsInterleukin-17Interleukin-2 Receptor alpha SubunitTubulin

Identifiers

PMID23325004
PMCPMC3549536
OpenAlexW1995391203

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.