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Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...
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Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
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Cells of the Innate Immune Response

The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
Phagocytes
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Updated: Jun 3, 2026

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
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Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Cytotoxic effects of lectins.

E Gorelik1

  • 1Department of Pathology, School of Medicine, University of Pitisburgh Cancer Institute. University of Pittsburgh, PA.

Methods in Molecular Medicine
|March 5, 2011
PubMed
Summary

Lectins can directly kill cells, a process distinct from lectin-dependent cell cytotoxicity. Studying lectin-resistant cells reveals mechanisms beyond simple carbohydrate loss, suggesting post-binding events influence cytotoxicity.

Area of Science:

  • Cell biology
  • Immunology
  • Biochemistry

Background:

  • Lectins interact with cells, causing proliferation or death.
  • Some lectins induce T-lymphocyte proliferation and cytotoxicity (lectin-dependent cell cytotoxicity, LDCC).
  • Other lectins directly kill cells without lymphocytes, termed direct lectin cytotoxicity.

Purpose of the Study:

  • To investigate the mechanisms of direct lectin cytotoxicity.
  • To analyze the mechanisms of lectin resistance in mammalian cells.
  • To understand the role of cell surface carbohydrates in lectin sensitivity and resistance.

Main Methods:

  • Isolation and characterization of lectin-resistant cell sublines from lectin-sensitive cell lines.
  • Analysis of cell surface carbohydrates, glycosyltransferase activity, and lectin binding in resistant variants.

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Real-time Cytotoxicity Assays in Human Whole Blood
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Real-time Cytotoxicity Assays in Human Whole Blood

Published on: November 7, 2014

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Last Updated: Jun 3, 2026

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes
12:12

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Real-time Cytotoxicity Assays in Human Whole Blood
08:27

Real-time Cytotoxicity Assays in Human Whole Blood

Published on: November 7, 2014

  • Investigation of post-binding events in lectin-mediated cell lysis.

    • Main Results:

    • Several lectins (Con A, PHA, WGA, GSlA, GSlB, LCA, ricin, abrin) exhibit direct cytotoxic properties.
    • Lectin-resistant variants were generated, with frequencies around 10(-5)-10(-6).
    • Some resistant variants lost specific glycosyltransferase activity and cell surface carbohydrates, while others did not, indicating post-binding resistance mechanisms.

    Conclusions:

    • Direct lectin cytotoxicity is a distinct mechanism of cell death mediated by various lectins.
    • Lectin resistance can arise from altered cell surface carbohydrates or post-binding events.
    • Tumor cell resistance to lectin cytotoxicity involves complex mechanisms beyond simple carbohydrate recognition.