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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.

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Related Experiment Video

Updated: Jun 10, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Apoptotic pathways in pemphigus.

Meryem Bektas1, Puneet Jolly, David S Rubenstein

  • 1Department of Dermatology, University of North Carolina-Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA.

Dermatology Research and Practice
|July 16, 2010
PubMed
Summary
This summary is machine-generated.

Pemphigus involves autoimmune blistering caused by antibodies attacking skin cell adhesion. While apoptosis isn't essential for blister formation, it may enhance the effects of pemphigus IgG on cell separation.

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Granulocyte-dependent Autoantibody-induced Skin Blistering

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Last Updated: Jun 10, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Detection and Isolation of Apoptotic Bodies to High Purity
12:17

Detection and Isolation of Apoptotic Bodies to High Purity

Published on: August 12, 2018

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Area of Science:

  • Dermatology
  • Immunology
  • Cell Biology

Background:

  • Pemphigus is an autoimmune blistering disease targeting desmosome cadherins.
  • Pathogenic IgG in pemphigus causes loss of cell-cell adhesion (acantholysis).
  • Apoptosis has been proposed as a contributing factor in pemphigus pathogenesis.

Purpose of the Study:

  • To review the current literature on the role of apoptosis in pemphigus.
  • To evaluate the contribution of apoptosis to the mechanism of pemphigus IgG-induced acantholysis.

Main Methods:

  • Literature review of studies investigating apoptosis in pemphigus.
  • Analysis of data on the involvement of proapoptotic proteins and signaling pathways.

Main Results:

  • Current evidence indicates apoptosis is not a prerequisite for blister induction in pemphigus.
  • Activation of proapoptotic proteins, such as caspase cysteine proteinases, is observed.
  • These apoptotic pathways may sensitize keratinocytes to the acantholytic actions of pemphigus IgG.

Conclusions:

  • Apoptosis is not essential for blister formation in pemphigus.
  • Activation of apoptotic pathways may modulate the severity of acantholysis induced by pemphigus autoantibodies.
  • Further research is needed to fully elucidate the interplay between apoptosis and pemphigus pathogenesis.