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Related Concept Videos

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.
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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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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
12:04

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Published on: November 1, 2015

The CD11b-integrin (ITGAM) and systemic lupus erythematosus.

S C Fagerholm1, M MacPherson, M J James

  • 1Medical Research Institute, Ninewells Hospital and Medical School, Institute of Biotechnology, University of Helsinki, Finland. s.c.fagerholm@dundee.ac.uk

Lupus
|June 12, 2013
PubMed
Summary

Genetic variations in the ITGAM gene, specifically rs1143679, are linked to systemic lupus erythematosus (SLE). This variant causes a dysfunctional Mac-1 integrin, impairing immune cell functions and potentially contributing to SLE development.

Keywords:
ITGAMSystemic lupus erythematosusintegrin

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Area of Science:

  • Immunology
  • Genetics
  • Rheumatology

Background:

  • The ITGAM gene encodes the CD11b chain of the Mac-1 integrin, a key immune cell receptor.
  • Genetic variations in ITGAM are strongly associated with systemic lupus erythematosus (SLE) risk.
  • A specific variant, rs1143679, leads to an arginine-to-histidine substitution in the Mac-1 integrin.

Purpose of the Study:

  • To review the immunological functions of the Mac-1 integrin.
  • To explore how genetic defects in Mac-1 may contribute to the development of SLE.
  • To understand the functional consequences of the rs1143679 variant.

Main Methods:

  • Review of existing literature on ITGAM gene, Mac-1 integrin function, and SLE.
  • Analysis of the functional impact of the arginine-to-histidine substitution at position 77.
  • Discussion of cellular adhesion, phagocytosis, and cytokine regulation by Mac-1.

Main Results:

  • The rs1143679 variant results in a dysfunctional Mac-1 integrin.
  • This dysfunctional integrin shows deficiencies in cell adhesion and phagocytosis.
  • The variant also impairs the ability to restrict inflammatory cytokine production in macrophages.

Conclusions:

  • Defects in the Mac-1 integrin due to ITGAM gene variations are implicated in SLE pathogenesis.
  • The rs1143679 variant's functional impairments provide a mechanistic link to SLE development.
  • Understanding these genetic and functional links is crucial for SLE research.