Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Special Features of Adaptive Immunity

Special Features of Adaptive Immunity

The adaptive immune system, a crucial component of the overall immune response, offers a highly specialized defense against pathogens. It involves specific cell types and features, enabling it to combat infections effectively and efficiently.
The primary cell types involved in adaptive immunity are T cells and B cells. Each type has a unique role in defending the body against pathogens. T cells are responsible for cell-mediated immunity. They identify and eliminate infected cells directly,...

Cell-mediated Immune Responses

Cell-mediated Immune Responses

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...

You might also read

Related Articles

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

Sort by

Same author

Glycoinformatic Profiling of Label-Free Intact Heparan Sulfate Oligosaccharides.

Molecular & cellular proteomics : MCP·2026

Same author

Urinary carbonic anhydrase 1 as a marker of hematuria in IgA nephropathy.

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association·2025

Same author

Trained innate immunity in response to nuclear antigens in systemic lupus erythematosus.

Journal of autoimmunity·2024

Same author

<i>Pneumocystis jirovecii</i> Pneumonia in Kidney Transplant Recipients Receiving Belatacept: A Report of Two Cases With Atypical Presentations.

Kidney medicine·2024

Same author

The roles of hyaluronan in kidney development, physiology and disease.

Nature reviews. Nephrology·2024

Same author

Trained immunity is regulated by T cell-induced CD40-TRAF6 signaling.

Cell reports·2024

Search research articles

Related Experiment Video

Updated: Apr 30, 2026

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

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

Published on: November 1, 2015

Breaking immunological tolerance in systemic lupus erythematosus.

Elmar Pieterse¹, Johan van der Vlag¹

¹Department of Nephrology, Radboud University Medical Center , Nijmegen , Netherlands.

Frontiers in Immunology

|May 1, 2014

Summary

Systemic lupus erythematosus (SLE) involves deregulated apoptosis and NETosis. Abnormal histone modifications from these cell death pathways may break immunological tolerance in SLE patients.

Keywords:

NETosis apoptosis histone modifications neutrophil systemic lupus erythematosus

More Related Videos

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

Published on: August 12, 2017

Murine Bilateral Renal Lymphadenectomy

Murine Bilateral Renal Lymphadenectomy

Published on: December 30, 2025

Related Experiment Videos

Last Updated: Apr 30, 2026

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

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

Published on: November 1, 2015

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients

Published on: August 12, 2017

Murine Bilateral Renal Lymphadenectomy

Murine Bilateral Renal Lymphadenectomy

Published on: December 30, 2025

Area of Science:

Immunology
Autoimmunity
Cell Biology

Background:

Systemic lupus erythematosus (SLE) is a complex autoimmune disease primarily affecting women of childbearing age.
SLE is characterized by immune complex deposition, leading to inflammation and multi-organ damage.
Dysregulation of apoptosis and NETosis has been observed in SLE.

Purpose of the Study:

To review the role of apoptosis and NETosis in SLE pathogenesis.
To discuss the impact of histone modifications in these cell death pathways on autoimmunity.
To explore how these abnormalities contribute to the loss of self-tolerance in SLE.

Main Methods:

Literature review of studies on apoptosis, NETosis, and histone modifications in SLE.
Analysis of current evidence linking cell death pathways to autoimmune responses.
Synthesis of findings on histone alterations and their role in immune tolerance breakdown.

Main Results:

Both apoptosis and NETosis appear to be deregulated in SLE.
Histone modifications induced by these cell death pathways are increasingly recognized as critical in autoimmunity.
Abnormalities in these processes are implicated in the loss of immunological tolerance.

Conclusions:

Aberrant apoptosis and NETosis, coupled with altered histone modifications, are key contributors to SLE pathogenesis.
Understanding these mechanisms is crucial for developing targeted therapies for SLE.
Further research into cell death pathways and histone regulation is warranted for SLE.