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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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An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
Complete Antigens
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Selectins01:25

Selectins

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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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Adherens Junctions01:24

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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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Intracellular Signaling Affects Focal Adhesions01:17

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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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Measurement of T Cell Alloreactivity Using Imaging Flow Cytometry
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Membrane attack complexes, endothelial cell activation, and direct allorecognition.

Guiyu Song1,2, Shaoxun Wang1,3, Mahsa Nouri Barkestani1

  • 1Section of Cardiovascular Medicine, Dept of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States.

Frontiers in Immunology
|October 10, 2022
PubMed
Summary
This summary is machine-generated.

The membrane attack complex (MAC) on endothelial cells (ECs) amplifies T cell responses in organ transplants. Inhibiting the complement cascade may prevent transplant rejection by targeting EC activation.

Keywords:
allorecognitionantibody-mediated rejectioncomplementendothelial celltransplant

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Area of Science:

  • Immunology
  • Transplantation Biology
  • Cellular Biology

Background:

  • Endothelial cells (ECs) are key players in the immune response during solid organ transplantation.
  • ECs present alloantigens to recipient T cells, initiating direct allorecognition.
  • Inflammatory mediators expressed by ECs critically shape T cell responses.

Purpose of the Study:

  • To review the molecular pathways of complement activation on ECs in transplantation.
  • To elucidate how the membrane attack complex (MAC) on ECs potentiates direct allorecognition.
  • To discuss complement-targeted therapeutics for preventing transplant rejection.

Main Methods:

  • Review of molecular pathways downstream of IgM- and IgG-mediated MAC assembly on ECs.
  • Analysis of MAC deposition effects on EC activation and signaling.
  • Discussion of clinical therapeutics targeting the complement pathway.

Main Results:

  • MAC assembly on ECs strengthens direct allorecognition by upregulating adhesion and costimulatory molecules.
  • MAC deposition generates 'signaling endosomes' that enhance EC activation and inflammatory molecule stability.
  • Complement activation on ECs promotes T cell-mediated inflammation in transplant rejection.

Conclusions:

  • The complement cascade, particularly MAC on ECs, is a critical driver of alloimmune responses in solid organ transplantation.
  • Understanding MAC-mediated EC activation pathways reveals potential therapeutic targets.
  • Inhibition of the complement pathway offers a promising strategy to prevent allograft rejection.