Evidence map›Paper›PMID 21345239›Full record

ArticleJournal of translational medicine2011

Alpha-1 antitrypsin protein and gene therapies decrease autoimmunity and delay arthritis development in mouse model.

Christian Grimstein, Young-Kook Choi, Clive H Wasserfall, Minoru Satoh, Mark A Atkinson, Mark L Brantly, Martha Campbell-Thompson, Sihong Song

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 86 citations in OpenAlex.

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  15. Review
  16. Serpins in cartilage and osteoarthritis: what do we know?Biochemical Society transactions · 2021
    Review
  17. Article
  18. Article
  19. Alpha-1 Antitrypsin Deficiency: a Rare Disease?Current allergy and asthma reports · 2020
    Review
  20. Potential Use of Alpha-1 Anti-trypsin in the Covid-19 Treatment.Frontiers in cell and developmental biology · 2020
    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

8 authors at 1 institution in 1 country.

Christian GrimsteinDepartment of Pharmaceutics, University of Florida, Gainesville, FL 32610, USA.
Young-Kook Choi
Clive H Wasserfall
Minoru Satoh
Mark A Atkinson
Mark L Brantly
Martha Campbell-Thompson
Sihong Song
University of Florida · US

Funding

Strategies for Sustained Effect of AAV-mediated Correction of Pompe DiseaseP01DK058327 · NIDDK · UNIVERSITY OF FLORIDA · PI BYRNE, BARRY J · 2000 to 2009
$11.0M
NIDDK NIH HHS DK58327
6 · The paper itself

Abstract

backgroundAlpha-1 antitrypsin (AAT) is a multi-functional protein that has anti-inflammatory and tissue protective properties. We previously reported that human AAT (hAAT) gene therapy prevented autoimmune diabetes in non-obese diabetic (NOD) mice and suppressed arthritis development in combination with doxycycline in mice. In the present study we investigated the feasibility of hAAT monotherapy for the treatment of chronic arthritis in collagen-induced arthritis (CIA), a mouse model of rheumatoid arthritis (RA).

methodsDBA/1 mice were immunized with bovine type II collagen (bCII) to induce arthritis. These mice were pretreated either with hAAT protein or with recombinant adeno-associated virus vector expressing hAAT (rAAV-hAAT). Control groups received saline injections. Arthritis development was evaluated by prevalence of arthritis and arthritic index. Serum levels of B-cell activating factor of the TNF-α family (BAFF), antibodies against both bovine (bCII) and mouse collagen II (mCII) were tested by ELISA.

resultsHuman AAT protein therapy as well as recombinant adeno-associated virus (rAAV8)-mediated hAAT gene therapy significantly delayed onset and ameliorated disease development of arthritis in CIA mouse model. Importantly, hAAT therapies significantly reduced serum levels of BAFF and autoantibodies against bCII and mCII, suggesting that the effects are mediated via B-cells, at least partially.

conclusionThese results present a new drug for arthritis therapy. Human AAT protein and gene therapies are able to ameliorate and delay arthritis development and reduce autoimmunity, indicating promising potential of these therapies as a new treatment strategy for RA.

Indexed as

Genetic Therapyalpha 1-AntitrypsinAnimalsArthritis, ExperimentalAutoantibodiesAutoimmunityB-Cell Activating FactorB-LymphocytesCattleCell LineCollagen Type IIDisease Models, AnimalDisease ProgressionHumansMaleMicealpha 1-AntitrypsinAutoantibodiesB-Cell Activating FactorCollagen Type II

Identifiers

PMID21345239
PMCPMC3050720
OpenAlexW2007798901

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Registered trials

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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.