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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
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Detecting Migration and Infiltration of Neutrophils in Mice
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Human neutrophils in auto-immunity.

Nathalie Thieblemont1, Helen L Wright2, Steven W Edwards2

  • 1INSERM, U1016, Institut Cochin, Paris, France; CNRS UMR 8104, 75014 Paris, France; Université Paris-Descartes, 75014, France; Center of Excellence, LABEX Inflamex, 75014, France.

Seminars in Immunology
|April 3, 2016
PubMed
Summary

Human neutrophils can trigger autoimmune diseases by releasing damage-causing molecules and neoepitopes. Neutrophil Extracellular Traps (NETs) are implicated in generating autoantibodies and driving conditions like vasculitis and rheumatoid arthritis.

Keywords:
ApoptosisLupusNeutrophilsPhagocytosisRheumatoid arthritisVasculitis

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Area of Science:

  • Immunology
  • Pathology
  • Cell Biology

Background:

  • Human neutrophils, crucial immune cells, can cause significant tissue damage during inflammation.
  • Activated neutrophils release reactive oxygen species (ROS), proteases, cytokines, and chemokines, influencing immune responses.
  • These cells can also generate neoepitopes, potentially breaking immune tolerance and leading to autoantibody production in autoimmune diseases.

Purpose of the Study:

  • To review the mechanisms by which neutrophils contribute to autoimmunity.
  • To elucidate the role of neutrophils in the pathogenesis of autoimmune diseases like vasculitis, rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE).
  • To discuss the involvement of Neutrophil Extracellular Traps (NETs) in neutrophil-mediated autoimmunity.

Main Methods:

  • Literature review of studies on neutrophil activation, autoantigen generation, and autoimmune diseases.
  • Analysis of the molecular processes involved in neoepitope formation, including ROS release, granule enzyme activity, and NETosis.
  • Examination of the role of neutrophil-derived molecules and NETs in diseases such as vasculitis, RA, and SLE.

Main Results:

  • Activated neutrophils release tissue-damaging molecules and neoepitopes that can trigger autoimmune responses.
  • Neutrophil Extracellular Traps (NETs), containing citrullinated proteins and granule enzymes, are identified as significant sources of autoantigens.
  • Neutrophils are implicated as effector cells in vascular damage in vasculitis and contribute to the pathology of RA and SLE.

Conclusions:

  • Neutrophils play a multifaceted role in the development and progression of autoimmune diseases.
  • NETs represent a critical link between neutrophil activation and the generation of auto-immunity.
  • Further research is needed to fully understand the complex role of neutrophils and NETs in autoimmunity and their therapeutic potential.