Evidence map›Paper›PMID 27226435›Full record

ArticleBlood2016

IL-4 rescues surface IgM expression in chronic lymphocytic leukemia.

Benchang Guo, Lu Zhang, Nicholas Chiorazzi, Thomas L Rothstein

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
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  7. NF-kB and the CLL microenvironment.Frontiers in oncology · 2023
    Review
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  9. Article
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  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Chronic Lymphocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2021
    Review
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  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Benchang GuoThe Feinstein Institute for Medical Research, Manhasset, NY;ORCID 0000-0002-8590-0635
Lu ZhangThe Feinstein Institute for Medical Research, Manhasset, NY;
Nicholas ChiorazziThe Feinstein Institute for Medical Research, Manhasset, NY; Department of Medicine, North Shore University Hospital, Manhasset, NY; Department of Medicine, and Department of Molecular Medicine, Hofstra Northwell School of Medicine, Hempstead, NY.ORCID 0000-0003-1023-6650
Thomas L RothsteinThe Feinstein Institute for Medical Research, Manhasset, NY; Department of Medicine, and Department of Molecular Medicine, Hofstra Northwell School of Medicine, Hempstead, NY.
Feinstein Institute for Medical Research · US

Funding

PHORBOL ESTER RESPONSIVE B LYMPHOCYTESR01AI029690 · NIAID · WESTERN MICHIGAN UNIV SCHOOL OF MEDICINE · PI ROTHSTEIN, THOMAS L · 1990 to 2019
$6.9M
B CELL REPERTOIRES IN CHRONIC LYMPHOCYTIC LEUKEMIAR01CA081554 · NCI · NORTH SHORE UNIVERSITY HOSPITAL · PI CHIORAZZI, NICHOLAS · 2000 to 2012
$2.7M
The essential role of RasGRP1 in B1 cell autoreactivity and autoimmunityR03AI115544 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI GUO, BENCHANG · 2015 to 2016
$169k
NCI NIH HHS R01 CA081554NIAID NIH HHS R01 AI029690NIAID NIH HHS R03 AI115544
6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) cells express poor levels of surface immunoglobulin (sIg), and many are minimally activated or anergic in response to B-cell receptor (BCR) crosslinking in vitro. Paradoxically, CLL cells in patients are highly activated through BCR signaling and expand in proliferation centers, suggesting that the function of sIg signaling is rescued. Here, we find that, compared with normal naïve B cells, CLL cells express a low level of total CD79b protein but normal levels of CD79a and IgM protein. Association of both CD79a and CD79b to IgM is markedly reduced. We further find that interleukin-4 (IL-4) markedly rescues CD79b and sIgM protein in CLL samples. These changes significantly enhance signaling in response to BCR crosslinking. Furthermore, we find that these changes are more pronounced in immunoglobulin heavy chain variable (IGHV)-unmutated CLL cells than IGHV-mutated CLL cells. The results described herein reveal that reduced sIgM is due to low expression of total CD79b protein in CLL cells. IL-4 substantially restores CD79b protein expression, sIgM expression, and BCR signaling.

Indexed as

CD79 AntigensCell LineGene Expression Regulation, NeoplasticHumansImmunoglobulin Heavy ChainsImmunoglobulin MInterleukin-4Leukemia, Lymphocytic, Chronic, B-CellNeoplasm ProteinsReceptors, Antigen, B-CellSignal TransductionCD79 AntigensCD79A protein, humanCD79B protein, humanIL4 protein, humanImmunoglobulin Heavy ChainsImmunoglobulin MInterleukin-4Neoplasm ProteinsReceptors, Antigen, B-Cell

Identifiers

PMID27226435
PMCPMC4965907
OpenAlexW2403449504

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.