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Related Concept Videos

Adherens Junctions01:24

Adherens Junctions

Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
The endothelial cells...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Immunoglobulin-like Cell Adhesion Molecules01:31

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
Ig-CAMs exhibit either homophilic binding (to other Ig-CAMs) or heterophilic binding (to other ligands such as integrins). While most Ig-CAMs...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
Disorders of Leukocytes01:27

Disorders of Leukocytes

Leukocyte disorders can lead to either leukopenia, characterized by an abnormally low leukocyte count, or leukocytosis, marked by a very high leukocyte number.
Leukopenia may result from bone marrow disorders, autoimmune diseases, and infectious diseases. For example, conditions such as multiple myeloma and aplastic anemia can impair the bone marrow's ability to produce adequate leukocytes. Similarly, autoimmune diseases like lupus and viral infections such as HIV can prompt the immune system...

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Related Experiment Video

Updated: Jun 23, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
08:50

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

Published on: April 9, 2018

Defects in the leukocyte adhesion cascade.

Amos Etzioni1

  • 1Meyer Children Hospital, Rappaport School of Medicine, Technion, Haifa, Israel. etzioni@rambam.health.gov.il

Clinical Reviews in Allergy & Immunology
|May 14, 2009
PubMed
Summary
This summary is machine-generated.

Leukocyte adhesion deficiencies (LAD) I, II, and III highlight the critical roles of specific adhesion molecules in immune responses and development. Genetic defects in these molecules lead to infections, developmental issues, and bleeding disorders.

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Assay of Adhesion Under Shear Stress for the Study of T Lymphocyte-Adhesion Molecule Interactions

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Last Updated: Jun 23, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
08:50

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

Published on: April 9, 2018

Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
09:14

Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes

Published on: June 13, 2014

Assay of Adhesion Under Shear Stress for the Study of T Lymphocyte-Adhesion Molecule Interactions
07:40

Assay of Adhesion Under Shear Stress for the Study of T Lymphocyte-Adhesion Molecule Interactions

Published on: June 29, 2016

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Leukocyte trafficking is essential for immune surveillance and inflammatory responses.
  • Adhesion molecules mediate leukocyte interaction with vascular endothelial cells during emigration.
  • Leukocyte adhesion deficiencies (LAD) reveal the critical functions of specific adhesion molecules.

Purpose of the Study:

  • To discuss the genetic defects underlying various adhesion molecule syndromes.
  • To elucidate the roles of beta(2)-integrins, selectins, and integrin activation in leukocyte function.
  • To highlight the clinical manifestations associated with different types of LAD.

Main Methods:

  • Review of genetic defects causing LAD I, II, and III.
  • Analysis of the molecular mechanisms of leukocyte adhesion and emigration.
  • Correlation of genetic deficiencies with clinical phenotypes.

Main Results:

  • LAD I, caused by beta(2)-integrin defects, leads to severe bacterial infections and often early childhood death.
  • LAD II, involving selectin receptors and ligands, results in less severe infections plus psychomotor and growth retardation.
  • LAD III, characterized by defective integrin activation, causes severe infections and bleeding tendencies.

Conclusions:

  • Genetic defects in adhesion molecules result in distinct clinical syndromes with varying degrees of immunodeficiency and developmental impairment.
  • Understanding these defects is crucial for diagnosing and managing patients with leukocyte adhesion deficiencies.
  • The study underscores the complex and vital role of adhesion molecules in both immunity and overall health.