Evidence map›Paper›PMID 28630091›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

B-1a Cells Protect Mice from Sepsis: Critical Role of CREB.

Monowar Aziz, Nichol E Holodick, Thomas L Rothstein, Ping Wang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.8field-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

53 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. B1 Cells for Life.Immunological reviews · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The transcription factor Bcl11a is essential for B-1a cell maintenance during aging.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. PD-L1Nature communications · 2025
    Article
  10. Article
  11. Article
  12. Identification of CD19Journal of inflammation research · 2025
    Article
  13. B-1a cells scavenge NETs to attenuate sepsis.Journal of leukocyte biology · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Destabilisation of T cell-dependent humoral immunity in sepsis.Clinical science (London, England : 1979) · 2024
    Review
  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

4 authors at 1 institution in 1 country.

Monowar AzizCenter for Immunology and Inflammation, Feinstein Institute for Medical Research, Manhasset, NY 11030; and.ORCID 0000-0002-8195-4505
Nichol E HolodickKarches Center for Oncology Research, Feinstein Institute for Medical Research, Manhasset, NY 11030.
Thomas L RothsteinKarches Center for Oncology Research, Feinstein Institute for Medical Research, Manhasset, NY 11030.
Ping WangCenter for Immunology and Inflammation, Feinstein Institute for Medical Research, Manhasset, NY 11030; and pwang@northwell.edu.
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
Novel Approaches to Maintaining Organ Function in SepsisR35GM118337 · NIGMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2016 to 2026
$5.2M
SEPSIS--MEDIATORS AND CARDIOVASCULAR RESPONSESR01GM057468 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, PING · 1998 to 2015
$3.8M
Modulation of Hepatocellular Function in SepsisR01GM053008 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, PING · 2001 to 2015
$3.7M
NIAID NIH HHS R01 AI029690NIGMS NIH HHS R01 GM053008NIGMS NIH HHS R01 GM057468NIGMS NIH HHS R35 GM118337
6 · The paper itself

Abstract

Bacterial sepsis is a serious life-threatening condition caused by an excessive immune response to infection. B-1 cells differ from conventional B-2 cells by their distinct phenotype and function. A subset of B-1 cells expressing CD5, known as B-1a cells, exhibits innate immune activity. Here we report that B-1a cells play a beneficial role in sepsis by mitigating exaggerated inflammation through a novel mechanism. Using a mouse model of bacterial sepsis, we found that the numbers of B-1a cells in various anatomical locations were significantly decreased. Adoptive transfer of B-1a cells into septic mice significantly attenuated systemic inflammation and improved survival, whereas B-1a cell-deficient CD19

Indexed as

Adoptive TransferAnimalsAntigens, CD19B-LymphocytesB-Lymphocyte SubsetsCyclic AMP Response Element-Binding ProteinDisease Models, AnimalInflammationInterleukin-10MiceSepsisAntigens, CD19CD19 antigen, mouseCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinIL10 protein, mouseInterleukin-10

Identifiers

PMID28630091
PMCPMC5531203
OpenAlexW2656613431

What OpenQuestion holds

Textmetadata
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.