Evidence map›Paper›PMID 25000533›Full record

ArticleCellular & molecular immunology2014

α1-antitrypsin increases interleukin-1 receptor antagonist production during pancreatic islet graft transplantation.

Avishag Abecassis, Ronen Schuster, Galit Shahaf, Eyal Ozeri, Ross Green, David E Ochayon, Peleg Rider, Eli C Lewis

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
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

29 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Association between α1-antitrypsin and acute coronary syndrome.Experimental and therapeutic medicine · 2020
    Article
  13. Review
  14. Article
  15. Anti-cytokines as a Strategy in Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Alpha-1-antitrypsin in cell and organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018
    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.

Avishag Abecassis
Ronen Schuster
Galit Shahaf
Eyal Ozeri
Ross Green
David E Ochayon
Peleg Rider
Eli C Lewis

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although islet transplantation for individuals with type 1 diabetes has been shown to yield superior blood glucose control, it remains inadequate for long-term control. This is partly due to islet injuries and stresses that can lead to beta cell loss. Inhibition of excess IL-1β activity might minimize islet injuries, thus preserving function. The IL-1 receptor antagonist (IL-1Ra), an endogenous inhibitor of IL-1β, protects islets from cytokine-induced necrosis and apoptosis. Therefore, an imbalance between IL-1β and IL-1Ra might influence the courses of allogeneic and autoimmune responses to islets. Our group previously demonstrated that the circulating serine-protease inhibitor human alpha-1-antitrypsin (hAAT), the levels of which increase in circulation during acute-phase immune responses, exhibits anti-inflammatory and islet-protective properties, as well as immunomodulatory activity. In the present study, we sought to determine whether the pancreatic islet allograft-protective activity of hAAT was mediated by IL-1Ra induction. Our results demonstrated that hAAT led to a 2.04-fold increase in IL-1Ra expression in stimulated macrophages and that hAAT-pre-treated islet grafts exhibited a 4.851-fold increase in IL-1Ra transcript levels, which were associated with a moderate inflammatory profile. Unexpectedly, islets that were isolated from IL-1Ra-knockout mice and pre-treated with hAAT before grafting into wild-type mice yielded an increase in intragraft IL-1Ra expression that was presumably derived from infiltrating host cells, albeit in the absence of hAAT treatment of the host. Indeed, hAAT-pre-treated islets generated hAAT-free conditioned medium that could induce IL-1Ra production in cultured macrophages. Finally, we demonstrated that hAAT promoted a distinct phosphorylation and nuclear translocation pattern for p65, a key transcription factor required for IL-1Ra expression.

Indexed as

Islets of Langerhans TransplantationActive Transport, Cell Nucleusalpha 1-AntitrypsinAnimalsCells, CulturedGraft RejectionHumansInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutPhosphorylationPostoperative Complicationsalpha 1-AntitrypsinInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinRela protein, mouseSERPINA1 protein, humanTranscription Factor RelA

Identifiers

PMID25000533
PMCPMC4085519

What OpenQuestion holds

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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.