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Related Concept Videos

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.
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...
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.
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...
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...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

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Related Experiment Video

Updated: Jun 19, 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

Apoptosis in psoriasis.

Marija Kastelan1, Larisa Prpić-Massari, Ines Brajac

  • 1University Department of Dermatology and Venereology, Rijeka University Hospital Center and School of Medicine, Kresimirova 42, HR-51000 Rijeka, Croatia. marijakastelan@yahoo.com

Acta Dermatovenerologica Croatica : ADC
|October 13, 2009
PubMed
Summary

Dysfunctional apoptosis, or programmed cell death, contributes to skin diseases like psoriasis. Psoriatic keratinocytes resist apoptosis, a key factor in this chronic inflammatory condition.

Area of Science:

  • Dermatology
  • Immunology
  • Cell Biology

Background:

  • Apoptosis (programmed cell death) is crucial for skin homeostasis, regulating keratinocyte proliferation and stratum corneum formation.
  • Dysfunctional apoptosis is implicated in various skin diseases, notably psoriasis, characterized by keratinocyte hyperproliferation and reduced apoptosis.
  • Psoriatic keratinocytes exhibit increased resistance to apoptosis, suggesting a key role in the disease's pathogenesis.

Purpose of the Study:

  • To review the role of different apoptotic pathways in the context of psoriasis.
  • To explore the mechanisms underlying keratinocyte apoptosis resistance in psoriasis.
  • To discuss the potential involvement of cell cytotoxicity in psoriasis pathogenesis.

Main Methods:

  • Literature review of studies on apoptosis in skin biology and psoriasis.

Related Experiment Videos

Last Updated: Jun 19, 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

  • Analysis of research on keratinocyte apoptosis regulation and dysregulation.
  • Examination of evidence regarding cytotoxic T cells and NK cells in psoriasis.

    • Main Results:

    • Psoriasis involves decreased keratinocyte apoptosis, contributing to epidermal hyperproliferation.
    • Psoriatic keratinocytes demonstrate enhanced resistance to apoptotic stimuli.
    • The precise role of cytotoxic CD8+ T cells and NK cells in psoriasis-related apoptosis remains under investigation.

    Conclusions:

    • Aberrant apoptosis is a significant factor in psoriasis development and progression.
    • Understanding apoptotic pathways offers potential therapeutic targets for psoriasis.
    • Further research is needed to elucidate the contribution of cell-mediated cytotoxicity to psoriasis.