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Selectins

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...

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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.
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Immunoglobulin-like Cell Adhesion Molecules

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.
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Cell Adhesion Molecules - Types and Functions

Cell Adhesion Molecules - Types and Functions

Cell adhesion molecules (CAMs) are pivotal to multicellularity and the coordinated functioning of tissues and organ systems. They enable physical interactions between cells and provide mechanical strength to tissues. They also function as receptors for signal transmission across the plasma membrane. The CAMs are broadly classified into four families - integrins, cadherins, selectins, and immunoglobulin-like CAMs (IgCAMs).
CAM Families
The Integrin family of proteins is primarily involved in a...

Cell Adhesion Molecules - Types and Functions

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Cell adhesion molecules (CAMs) are pivotal to multicellularity and the coordinated functioning of tissues and organ systems. They enable physical interactions between cells and provide mechanical strength to tissues. They also function as receptors for signal transmission across the plasma membrane. The CAMs are broadly classified into four families - integrins, cadherins, selectins, and immunoglobulin-like CAMs (IgCAMs).
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Related Experiment Video

Updated: May 25, 2026

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

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

Published on: April 9, 2018

Leukocyte adhesion deficiencies.

Suhair Hanna¹, Amos Etzioni

¹Meyer Children's Hospital, Rambam Campus, Rappaport Faculty of Medicine, Technion, Haifa, Israel.

Annals of the New York Academy of Sciences

|January 27, 2012

Summary

Leukocyte adhesion deficiencies (LAD) disrupt immune surveillance. This study details genetic defects in LAD I, II, and III, affecting leukocyte adhesion cascade phases, but notes no models for transmigration defects exist.

Area of Science:

Immunology
Cell Biology
Genetics

Background:

Leukocyte trafficking is vital for immune surveillance, involving a multi-step adhesion cascade.
Leukocyte Adhesion Deficiencies (LAD) impair this process, with distinct genetic causes.
Existing models cover defects in adhesion and rolling phases of the cascade.

Purpose of the Study:

To review the genetic basis of Leukocyte Adhesion Deficiency (LAD) types I, II, and III.
To highlight the molecular mechanisms underlying these distinct leukocyte adhesion defects.
To identify the gap in current models concerning the transmigration phase of leukocyte adhesion.

Main Methods:

Literature review of genetic mutations causing LAD.
Analysis of molecular defects in integrin function and ligand expression.

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Published on: April 9, 2018

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Comparative analysis of known LAD models and their affected cascade phases.

Main Results:

LAD I results from beta 2 integrin gene mutations affecting firm adhesion.
LAD II stems from fucose transporter defects, impacting Sialyl Lewis X expression and rolling.
LAD III involves kindlin-3 mutations, crucial for integrin activation (second phase).

Conclusions:

Genetic defects in LAD I, II, and III disrupt specific, sequential phases of the leukocyte adhesion cascade.
Kindlin-3 mutations represent a newly identified cause of LAD III, affecting integrin activation.
A significant gap exists, with no described human or animal models for defects in the transmigration phase of leukocyte adhesion.