Evidence map›Paper›PMID 22262657›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Natural IgM anti-leukocyte autoantibodies attenuate excess inflammation mediated by innate and adaptive immune mechanisms involving Th-17.

Peter I Lobo, Amandeep Bajwa, Kailo H Schlegel, John Vengal, Sang J Lee, Liping Huang, Hong Ye, Umesh Deshmukh, Tong Wang, Hong Pei and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. 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
1.4field-weighted citation impact, top 20% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The five dimensions of B cell tolerance.Immunological reviews · 2019
    Review
  10. Review
  11. Review
  12. B Regulatory Cells: Players in Pregnancy and Early Life.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. B Cells, Antibodies, and More.Clinical journal of the American Society of Nephrology : CJASN · 2016
    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

11 authors at 1 institution in 1 country.

Peter I LoboDivision of Nephrology, Center for Immunity, Inflammation and Regenerative Medicine, University of Virginia, Charlottesville, VA 22908, USA. pil@virginia.edu
Amandeep Bajwa
Kailo H Schlegel
John Vengal
Sang J Lee
Liping Huang
Hong Ye
Umesh Deshmukh
Tong Wang
Hong Pei
Mark D Okusa
University of Virginia · US

Funding

Sphingolipids in Acute Kidney Injury and Disease ProgressionR01DK085259 · NIDDK · UNIVERSITY OF VIRGINIA · PI OKUSA, MARK DOUGLAS · 2010 to 2023
$5.0M
Naturally Occurring IgM Anti-Leucocyte Autoantibodies Protect Against Renal IRIR01DK083406 · NIDDK · UNIVERSITY OF VIRGINIA · PI LOBO, PETER, OKUSA, MARK DOUGLAS · 2010 to 2014
$2.1M
Sphingosine 1 phosphate receptors 1 and 3 as novel targets in transplantationK01DK091444 · NIDDK · UNIVERSITY OF VIRGINIA · PI BAJWA, AMANDEEP · 2012 to 2016
$579k
Nanotherapeutics for acute kidney injuryR21DK093841 · NIDDK · UNIVERSITY OF VIRGINIA · PI KLIBANOV, ALEXANDER L, OKUSA, MARK DOUGLAS · 2012 to 2013
$425k
IgM Antileucocyte Autoantibodies Inhibit Kidney Allograft RejectionsR21DK077281 · NIDDK · UNIVERSITY OF VIRGINIA · PI LOBO, PETER · 2009 to 2010
$414k
NIDDK NIH HHS K01 DK091444NIDDK NIH HHS R01 DK083406NIDDK NIH HHS R01DK083406-01A1NIDDK NIH HHS R01 DK085259NIDDK NIH HHS R21 DK077281NIDDK NIH HHS R21DK077281-01A2NIDDK NIH HHS R21 DK093841
6 · The paper itself

Abstract

Little is known about the function of natural IgM autoantibodies, especially that of IgM anti-leukocyte autoantibodies (IgM-ALA). Natural IgM-ALA are present at birth and characteristically increase during inflammatory and infective conditions. Our prior clinical observations and those of other investigators showing fewer rejections in renal and cardiac allografts transplanted into recipients with high levels of IgM-ALA led us to investigate whether IgM-ALA regulate the inflammatory response. In this article, we show that IgM, in physiologic doses, inhibit proinflammatory cells from proliferating and producing IFN-γ and IL-17 in response to alloantigens (MLR), anti-CD3, and the glycolipid α-galactosyl ceramide. We showed in an IgM knockout murine model, with intact B cells and regulatory T cells, that there was more severe inflammation and loss of function in the absence of IgM after renal ischemia reperfusion injury and cardiac allograft rejection. Replenishing IgM in IgM knockout mice or increasing the levels of IgM-ALA in wild-type B6 mice significantly attenuated the inflammation in both of these inflammatory models that involve IFN-γ and IL-17. The protective effect on renal ischemia reperfusion injury was not observed using IgM preadsorbed with leukocytes to remove IgM-ALA. We provide data to show that the anti-inflammatory effect of IgM is mediated, in part, by inhibiting TLR-4-induced NF-κB translocation into the nucleus and inhibiting differentiation of activated T cells into Th-1 and Th-17 cells. These observations highlight the importance of IgM-ALA in regulating excess inflammation mediated by both innate and adaptive immune mechanisms and where the inflammatory response involves Th-17 cells that are not effectively regulated by regulatory T cells.

Indexed as

Adaptive ImmunityAnimalsAutoantibodiesCD3 ComplexCell DifferentiationGalactosylceramidesImmunity, InnateImmunoglobulin MInflammationInterferon-gammaInterleukin-17IsoantigensLeukocytesLymphocyte ActivationMiceMice, Inbred BALB Calpha-galactosylceramideAutoantibodiesCD3 ComplexGalactosylceramidesImmunoglobulin MInterferon-gammaInterleukin-17IsoantigensNF-kappa BTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID22262657
PMCPMC3273570
OpenAlexW2102973005

What OpenQuestion holds

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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.