Evidence map›Paper›PMID 16045741›Full record

ArticleClinical and experimental immunology2005

An increased MRP8/14 expression and adhesion, but a decreased migration towards proinflammatory chemokines of type 1 diabetes monocytes.

G Bouma, J M C Coppens, W-K Lam-Tse, W Luini, K Sintnicolaas, W H Levering, S Sozzani, H A Drexhage, M A Versnel

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In one paragraph

Article in Clinical and experimental immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 43 citations in OpenAlex.

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  7. Local and Systemic Immune Dysregulation Alters Glioma Growth in Hyperglycemic Mice.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
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  17. Mycelial forms of Coccidioides spp. in the parasitic phase associated to pulmonary coccidioidomycosis with type 2 diabetes mellitus.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2008
    Article
  18. Type 1 diabetes promotes disruption of advanced atherosclerotic lesions in LDL receptor-deficient mice.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  19. Article
  20. 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

9 authors at 4 institutions in 2 countries.

G BoumaDepartment of Immunology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands. g.bouma@ich.ucl.ac.uk
J M C Coppens
W-K Lam-Tse
W Luini
K Sintnicolaas
W H Levering
S Sozzani
H A Drexhage
M A Versnel
Erasmus MC · NLSanquin · NLMario Negri Institute for Pharmacological Research · ITUniversity of Brescia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the early development of type 1 diabetes macrophages and dendritic cells accumulate around the islets of Langerhans at sites of fibronectin expression. It is thought that these macrophages and dendritic cells are derived from blood monocytes. Previously, we showed an increased serum level of MRP8/14 in type 1 diabetes patients that induced healthy monocytes to adhere more strongly to fibronectin (FN). Here we show that MRP8/14 is expressed and produced at a higher level by type 1 diabetes monocytes, particularly after adhesion to FN, creating a positive feedback mechanism for a high fibronectin-adhesive capacity. Also adhesion to endothelial cells was increased in type 1 diabetes monocytes. Despite this increased adhesion the transendothelial migration of monocytes of type 1 diabetes patients was decreased towards the proinflammatory chemokines CCL2 and CCL3. Because non-obese diabetic (NOD) mouse monocytes show a similar defective proinflammatory migration, we argue that an impaired monocyte migration towards proinflammatory chemokines might be a hallmark of autoimmune diabetes. This hampered monocyte response to proinflammatory chemokines questions whether the early macrophage and dendritic cell accumulation in the diabetic pancreas originates from an inflammatory-driven influx of monocytes. We also show that the migration of type 1 diabetes monocytes towards the lymphoid tissue-related CCL19 was increased and correlated with an increased CCR7 surface expression on the monocytes. Because NOD mice show a high expression of these lymphoid tissue-related chemokines in the early pancreas it is more likely that the early macrophage and dendritic cell accumulation in the diabetic pancreas is related to an aberrant high expression of lymphoid tissue-related chemokines in the pancreas.

Indexed as

AdultCalgranulin ACalgranulin BCase-Control StudiesCell AdhesionChemotaxis, LeukocyteCytokinesDiabetes Mellitus, Type 1Enzyme-Linked Immunosorbent AssayFemaleFibronectinsFlow CytometryHumansImmunophenotypingMaleMonocytesCalgranulin ACalgranulin BCytokinesFibronectins

Identifiers

PMID16045741
PMCPMC1809454
OpenAlexW1973096129

What OpenQuestion holds

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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.