Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Editorial Expression of Concern: N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl<sup>+</sup> cells by endothelial nitric oxide synthase-mediated production.

Apoptosis : an international journal on programmed cell death·2026
Same author

Angiotensin-converting enzyme overexpression in mouse neutrophils prevents Alzheimer's-like cognitive decline.

Frontiers in immunology·2026
Same author

Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth.

Signal transduction and targeted therapy·2026
Same author

A Method to Enrich Functional Human Paneth Cells in Induced Pluripotent Stem Cell-Derived Intestinal Organoids.

Cellular and molecular gastroenterology and hepatology·2026
Same author

EpCAM silencing suppresses aggressive phenotypes and induces partial redifferentiation in anaplastic thyroid cancer cells.

PloS one·2026
Same author

Deciphering the Impact of RAC1-SPTAN1 in ARPKD Cystogenesis Using Multifaceted Models.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Related Experiment Video

Updated: Jul 4, 2025

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
12:04

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

17.6K

Distinct RBC alloantibody responses in type 1 interferon-dependent and -independent lupus mouse models.

Kausik Paul1, Rosario Hernández-Armengol1, June Young Lee1

  • 1Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, United States.

Frontiers in Immunology
|January 30, 2024
PubMed
Summary

Type I interferons (IFNα/β) drive red blood cell (RBC) alloantibody production in lupus models, not the autoimmune condition itself. This suggests patients with systemic lupus erythematosus (SLE) expressing IFN signatures may need personalized transfusion strategies.

Keywords:
MRL-lprRBC alloimmunizationautoimmunitylupustransfusiontype 1 interferons

More Related Videos

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

2.9K
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

114

Related Experiment Videos

Last Updated: Jul 4, 2025

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice
12:04

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

17.6K
Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

2.9K
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

114

Area of Science:

  • Immunology
  • Transfusion Medicine
  • Rheumatology

Background:

  • Red blood cell (RBC) alloimmunization can occur during transfusions due to exposure to non-ABO antigens.
  • Alloimmunization is more frequent in inflammatory conditions and autoimmune diseases, but mechanisms remain unclear.
  • Systemic lupus erythematosus (SLE) patients often exhibit type I interferon (IFNα/β) activity and express IFN-stimulated genes (ISGs).

Purpose of the Study:

  • To investigate whether type I interferons (IFNα/β) or a lupus-like phenotype drives RBC alloimmune responses.
  • To compare alloimmune responses in IFNα/β-dependent and independent lupus mouse models.

Main Methods:

  • Utilized pristane-induced and MRL-lpr lupus mouse models to assess RBC alloimmunization.
  • Administered KEL antigen-expressing murine RBCs to induce alloantibody production.
  • Measured interferon-stimulated gene (ISG) expression and anti-KEL IgG levels.
  • Administered recombinant IFNα to MRL-lpr mice.

Main Results:

  • Pristane-treated mice showed high ISG levels and produced anti-KEL IgG, while MRL-lpr mice had low ISG levels and minimal anti-KEL IgG.
  • A lupus-like phenotype alone did not induce significant RBC alloantibody production.
  • Recombinant IFNα treatment enhanced alloimmunization in MRL-lpr mice.

Conclusions:

  • Type I interferons (IFNα/β), not just autoimmunity, are critical drivers of RBC alloimmune responses in lupus models.
  • IFNα/β gene signatures may identify SLE patients at higher risk for RBC alloantibodies.
  • Findings suggest a need for personalized transfusion protocols for SLE patients with IFN signatures.