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Immunoglobulin-like Cell Adhesion Molecules01:31

Immunoglobulin-like Cell Adhesion Molecules

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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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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.
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Cell Adhesion Molecules - Types and Functions01:20

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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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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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Selectins01:25

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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,...
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Static Adhesion Assay for the Study of Integrin Activation in T Lymphocytes
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Molecular mechanisms regulating CD13-mediated adhesion.

Mallika Ghosh1, Claire Gerber, M Mamunur Rahman

  • 1Center for Vascular Biology, University of Connecticut Health Center, Farmington, CT, USA.

Immunology
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Summary

CD13 expression on myeloid cells is crucial for their trafficking to inflammatory sites. Lack of CD13 impairs immune cell infiltration, impacting inflammatory responses and suggesting therapeutic potential.

Keywords:
adhesion moleculescell traffickinginflammationtransgenic/knockout mice

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Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • CD13 (Aminopeptidase N) is a metalloproteinase involved in cellular functions.
  • It is upregulated on endothelial cells during inflammation and mediates monocyte adhesion.
  • CD13 expression is enriched on pro-inflammatory monocyte subsets.

Purpose of the Study:

  • To investigate the role of CD13 in regulating immune cell trafficking during inflammation.
  • To dissect the mechanisms of CD13-dependent cell migration.
  • To identify the molecular domain of CD13 responsible for adhesion.

Main Methods:

  • Utilized a murine model of thioglycollate-induced sterile peritonitis.
  • Employed global CD13 knockout (CD13(KO)) mice.
  • Performed adoptive transfer experiments with wild-type and CD13(KO) myeloid cells.
  • Analyzed immune cell populations in peritoneal exudates.
  • Used chimeric CD13 molecules to map functional domains.

Main Results:

  • Peritoneal monocytes, macrophages, and dendritic cells were significantly reduced in CD13(KO) mice.
  • Adoptive transfer showed fewer CD13(KO) or CD13-blocked cells in inflammatory infiltrates.
  • Both monocytic and endothelial CD13 were found to contribute to cell trafficking.
  • The C-terminal domain of CD13 mediates cell adhesion.

Conclusions:

  • CD13 expression confers a competitive advantage for myeloid cell trafficking to inflammatory sites.
  • Aberrant myeloid cell subset trafficking in CD13(KO) mice results from impaired CD13 function.
  • This study defines molecular mechanisms of CD13-mediated immune cell migration.