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Related Concept Videos

Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Complement System01:27

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
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...
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...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...

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Updated: Jun 26, 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

Programmed necrotic cell death induced by complement involves a Bid-dependent pathway.

Lea Ziporen1, Natalie Donin, Taisia Shmushkovich

  • 1Department of Cell and Developmental Biology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.

Journal of Immunology (Baltimore, Md. : 1950)
|December 26, 2008
PubMed
Summary
This summary is machine-generated.

The membrane attack complex (MAC) triggers cell death, but Bid knockout cells show resistance. This suggests Bid plays a key role in MAC-induced cell death pathways.

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Evaluation of Caspase Activation to Assess Innate Immune Cell Death
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Evaluation of Caspase Activation to Assess Innate Immune Cell Death

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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

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • The complement system's membrane attack complex (MAC) induces necrotic cell death.
  • Bcl-2 is known to protect cells against MAC-induced necrosis.

Purpose of the Study:

  • To investigate the role of the proapoptotic protein Bid in MAC-induced cytotoxicity.
  • To understand the mechanisms by which MAC induces cell death.

Main Methods:

  • Utilized Bid knockout (Bid-/-) mouse embryonic fibroblasts (MEF) and primary fibroblasts.
  • Employed small interfering RNA (siRNA) for Bid silencing in various cell lines.
  • Analyzed complement protein deposition (C3, C9) and expression of complement inhibitors (Crry, CD59).
  • Assessed cell lysis using toxic agents and measured Bid cleavage in response to MAC.

Main Results:

  • Bid-/- fibroblasts exhibited significantly lower damage and lysis from complement compared to wild-type (WT) cells.
  • Bid silencing conferred resistance to complement-mediated lysis in mouse, K562, and Jurkat cells.
  • Bid-/- MEF showed resistance to other pore-forming toxins like streptolysin O, melittin, and A23187.
  • Less C3 and C9 deposition occurred on Bid-/- cells despite reduced complement inhibitor expression.
  • Bid cleavage was observed in WT MEF upon MAC exposure and was reduced by a pan-caspase inhibitor, correlating with reduced cell lysis.

Conclusions:

  • Complement MAC activates distinct cell death pathways.
  • One pathway involves caspases and Bid, while another is Bid-independent.
  • Bid plays a crucial role in mediating MAC-induced cytotoxicity.