Evidence map›Paper›PMID 26218624›Full record

ArticlemAbs2015

Targeting CD64 mediates elimination of M1 but not M2 macrophages in vitro and in cutaneous inflammation in mice and patient biopsies.

Dmitrij Hristodorov, Radoslav Mladenov, Verena von Felbert, Michael Huhn, Rainer Fischer, Stefan Barth, Theo Thepen

Open access · goldAbstract read
In one paragraph

Article in mAbs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Crosstalk between CD64EMBO molecular medicine · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Macrophage Phenotyping in Atherosclerosis by Proteomics.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
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  20. 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

7 authors at 3 institutions in 3 countries.

Dmitrij Hristodorova Department of Experimental Medicine and Immunotherapy ; Institute of Applied Medical Engineering; University Hospital; RWTH Aachen University ; Aachen , Germany.
Radoslav Mladenov
Verena von Felbert
Michael Huhn
Rainer Fischer
Stefan Barth
Theo Thepen
RWTH Aachen University · DEFraunhofer Institute for Molecular Biology and Applied Ecology · DEInstitute of Molecular Biotechnology · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are key players in controlling the immune response that can adapt to microenvironmental signals. This results in distinct polarization states (classical M1 or alternative M2), that play a differential role in immune regulation. In general, the M1 contribute to onset of inflammation, whereas the M2 orchestrate resolution and repair, whereby failure to switch from predominantly M1 to M2 reinforces a pro-inflammatory environment and chronic inflammation. Here, we show selective elimination of M1 macrophages in vitro by a range of CD64-targeted immunotoxins, including H22(scFv)-ETA'. After re-polarization of already polarized macrophages, still only M1 polarization showed sensitivity toward CD64-directed immunotoxins. The selectivity for M1 was found linked to reduced endosomal protease activity in M1 macrophages as demonstrated by inhibition of endosomal proteases. Using the H22(scFv)-ETA' in a transgenic mouse model for chronic cutaneous inflammation, the M1 specificity was confirmed in vivo and a beneficial effect on inflammation demonstrated. Also ex vivo on skin biopsies from atopic dermatitis and diabetes type II patients with chronically-inflamed skin, a clear M1 specific effect was found. This indicates the potential relevance for human application. Our data show that targeting M1 macrophages through CD64 can be instrumental in developing novel intervention strategies for chronic inflammatory conditions.

Indexed as

AnimalsCell DifferentiationDermatitisEnzyme-Linked Immunosorbent AssayFlow CytometryHumansImmunohistochemistryMacrophagesMaleMiceMice, Inbred C57BLMice, NudeMice, TransgenicReceptors, IgGReceptors, IgGCD64chronic inflammationH22immunotherapypolarized macrophages

Identifiers

PMID26218624
PMCPMC4622427
OpenAlexW1856995660

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.