Evidence map›Paper›PMID 26209628›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Selective Targeting of a Disease-Related Conformational Isoform of Macrophage Migration Inhibitory Factor Ameliorates Inflammatory Conditions.

Michael Thiele, Randolf J Kerschbaumer, Frederick W K Tam, Dirk Völkel, Patrice Douillard, Alexander Schinagl, Harald Kühnel, Jennifer Smith, John P McDaid, Gurjeet Bhangal and 14 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. 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
2.2field-weighted citation impact, top 12% 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, 60 citations in OpenAlex.

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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

24 authors at 8 institutions in 3 countries.

Michael ThieleBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Randolf J KerschbaumerBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria; randolf_kerschbaumer@baxter.com.
Frederick W K TamImperial College Renal and Transplant Centre, Hammersmith Hospital, London W12 0NN, United Kingdom;
Dirk VölkelBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Patrice DouillardBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Alexander SchinaglBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Harald KühnelBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Jennifer SmithImperial College Renal and Transplant Centre, Hammersmith Hospital, London W12 0NN, United Kingdom;
John P McDaidImperial College Renal and Transplant Centre, Hammersmith Hospital, London W12 0NN, United Kingdom;
Gurjeet BhangalImperial College Renal and Transplant Centre, Hammersmith Hospital, London W12 0NN, United Kingdom;
Mei-Ching YuImperial College Renal and Transplant Centre, Hammersmith Hospital, London W12 0NN, United Kingdom;
Charles D PuseyImperial College Renal and Transplant Centre, Hammersmith Hospital, London W12 0NN, United Kingdom;
H Terence CookImperial College Renal and Transplant Centre, Hammersmith Hospital, London W12 0NN, United Kingdom;
Josef KovarikDepartment of Nephrology, Wilhelminenspital, 1160 Vienna, Austria;
Erica MagelkyDepartment of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215;
Atul BhanDepartment of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02214;
Manfred RiegerBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Geert C MuddeBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Hartmut EhrlichBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Bernd JilmaDepartment of Clinical Pharmacology, Medical University Vienna, 1090 Vienna, Austria; and.
Herbert TilgDepartment of Internal Medicine I, Endocrinology, Gastroenterology & Metabolism, Medical University Innsbruck, 6020 Innsbruck, Austria.
Alexander MoschenDepartment of Internal Medicine I, Endocrinology, Gastroenterology & Metabolism, Medical University Innsbruck, 6020 Innsbruck, Austria.
Cox TerhorstDepartment of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215;
Friedrich ScheiflingerBaxter Biomedical Research Center, Baxter Innovations GmbH, 2304 Orth/Donau, Austria;
Hammersmith Hospital · GBBaxter (Austria) · ATBaxter (United States) · USHarvard University · USInnsbruck Medical University · ATMassachusetts General Hospital · USMedical University of Vienna · ATWilhelminen Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage migration inhibitory factor (MIF), a proinflammatory cytokine and counterregulator of glucocorticoids, is a potential therapeutic target. MIF is markedly different from other cytokines because it is constitutively expressed, stored in the cytoplasm, and present in the circulation of healthy subjects. Thus, the concept of targeting MIF for therapeutic intervention is challenging because of the need to neutralize a ubiquitous protein. In this article, we report that MIF occurs in two redox-dependent conformational isoforms. We show that one of the two isoforms of MIF, that is, oxidized MIF (oxMIF), is specifically recognized by three mAbs directed against MIF. Surprisingly, oxMIF is selectively expressed in the plasma and on the cell surface of immune cells of patients with different inflammatory diseases. In patients with acute infections or chronic inflammation, oxMIF expression correlated with inflammatory flare-ups. In addition, anti-oxMIF mAbs alleviated disease severity in mouse models of acute and chronic enterocolitis and improved, in synergy with glucocorticoids, renal function in a rat model of crescentic glomerulonephritis. We conclude that oxMIF represents the disease-related isoform of MIF; oxMIF is therefore a new diagnostic marker for inflammation and a relevant target for anti-inflammatory therapy.

Indexed as

AnimalsAntibodies, MonoclonalBlotting, WesternDexamethasoneDisease Models, AnimalEnterocolitisFlow CytometryGlomerulonephritisGlucocorticoidsHumansInflammationMacrophage Migration-Inhibitory FactorsMaleMice, Inbred C57BLMice, KnockoutMolecular Targeted TherapyAntibodies, MonoclonalDexamethasoneGlucocorticoidsMacrophage Migration-Inhibitory FactorsProtein Isoforms

Identifiers

PMID26209628
PMCPMC4543907
OpenAlexW2171591425

What OpenQuestion holds

Textmetadata
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.