Evidence map›Paper›PMID 37619906›Full record

ReviewAutoimmunity reviews2023

Islet beta-cells and intercellular adhesion molecule-1 (ICAM-1): Integrating immune responses that influence autoimmunity and graft rejection.

Thomas M Martin, Susan J Burke, Clive H Wasserfall, J Jason Collier

Open access · greenAbstract readReview
In one paragraph

Review in Autoimmunity reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 17 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

4 authors at 3 institutions in 1 country.

Thomas M MartinLaboratory of Islet Biology and Inflammation, Pennington Biomedical Research Center, Baton Rouge, LA 70808, United States of America; Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, United States of America.
Susan J BurkeLaboratory of Immunogenetics, Pennington Biomedical Research Center, Baton Rouge, LA 70808, United States of America.
Clive H WasserfallDepartment of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL 32610, United States of America.
J Jason CollierLaboratory of Islet Biology and Inflammation, Pennington Biomedical Research Center, Baton Rouge, LA 70808, United States of America; Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, United States of America. Electronic address: Jason.collier@pbrc.edu.
Pennington Biomedical Research Center · USLouisiana State University · USUniversity of Florida · US

Funding

The role of maternal obesity-driven inflammation and adverse pregnancy outcomes in a mouse model of preeclampsiaP20GM135002 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Jacqueline M Stephens · 2020 to 2026
$18.4M
Training in Botanical Approaches to Combat Metabolic SyndromeT32AT004094 · NCCIH · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI BRANTLEY, PHILLIP J, STEPHENS, JACQUELINE M · 2009 to 2024
$5.7M
SGK1 is a regulator of islet beta cell mass and secretory functionR01DK123183 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI COLLIER, JAMES JASON · 2020 to 2024
$1.8M
Development of Mice with Conditional ICAM-1 DeletionR03AI151920 · NIAID · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI COLLIER, JAMES JASON · 2020 to 2021
$153k
NCCIH NIH HHS T32 AT004094NIAID NIH HHS R03 AI151920NIDDK NIH HHS R01 DK123183NIGMS NIH HHS P20 GM135002
6 · The paper itself

Abstract

Type 1 diabetes (T1D) develops due to autoimmune targeting of the pancreatic islet β-cells. Clinical symptoms arise from reduced insulin in circulation. The molecular events and interactions between discrete immune cell populations, infiltration of such leukocytes into pancreatic and islet tissue, and selective targeting of the islet β-cells during autoimmunity and graft rejection are not entirely understood. One protein central to antigen presentation, priming of immune cells, trafficking of leukocytes, and vital for leukocyte effector function is the intercellular adhesion molecule-1 (ICAM-1). The gene encoding ICAM-1 is transcriptionally regulated and rapidly responsive (i.e., within hours) to pro-inflammatory cytokines. ICAM-1 is a transmembrane protein that can be glycosylated; its presence on the cell surface provides co-stimulatory functions for immune cell activation and stabilization of cell-cell contacts. ICAM-1 interacts with the β2-integrins, CD11a/CD18 (LFA-1) and CD11b/CD18 (Mac-1), which are present on discrete immune cell populations. A whole-body ICAM-1 deletion protects NOD mice from diabetes onset, strongly implicating this protein in autoimmune responses. Since several different cell types express ICAM-1, its biology is fundamentally essential for various physiological and pathological outcomes. Herein, we review the role of ICAM-1 during both autoimmunity and islet graft rejection to understand the mechanism(s) leading to islet β-cell death and dysfunction that results in insufficient circulating quantities of insulin to control glucose homeostasis.

Indexed as

AutoimmunityGraft RejectionIntercellular Adhesion Molecule-1Islets of LangerhansAnimalsHumansInsulinsLymphocyte Function-Associated Antigen-1Macrophage-1 AntigenMiceMice, Inbred NODICAM1 protein, humanInsulinsIntercellular Adhesion Molecule-1Lymphocyte Function-Associated Antigen-1Macrophage-1 AntigenAutoimmunityICAM-1InflammationPancreatic isletType 1 diabetes

Identifiers

PMID37619906
PMCPMC10543623
OpenAlexW4386056736

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.