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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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Neurotransmitters play a crucial role in the communication between neurons in the autonomic nervous system. Neurons in the autonomic nervous system can be cholinergic or adrenergic depending on the neurotransmitters synthesized. Cholinergic neurons use acetylcholine as their primary neurotransmitter. This includes all the preganglionic fibers of the sympathetic and pre- and postganglionic fibers of the parasympathetic nervous systems. In addition, neurons of the somatic nervous system also use...
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Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
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Neurotransmitters arrive to control systemic autoimmunity.

Marc Scherlinger1, George C Tsokos2

  • 1Centre National de Référence des Maladies Auto-Immunes et Systémiques Rares, Est/Sud-Ouest (RESO), France; Service de rhumatologie, Centre Hospitalier Universitaire de Strasbourg, 1 avenue Molière, 67098 Strasbourg, France; Laboratoire d'ImmunoRhumatologie Moléculaire, Institut national de la santé et de la recherche médicale (INSERM) UMR_S 1109, Strasbourg, France.

Cell Metabolism
|May 3, 2023
PubMed
Summary
This summary is machine-generated.

In systemic lupus erythematosus, acetylcholine from splenic stromal cells alters B cell metabolism. This promotes B cell autoreactivity and disease progression in both humans and mice.

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Area of Science:

  • Immunology
  • Cell Biology
  • Metabolism

Background:

  • The immune cell microenvironment is critical for regulating immune cell function.
  • Aberrant immune cell function characterizes autoimmune diseases like systemic lupus erythematosus (SLE).

Purpose of the Study:

  • To investigate the role of splenic stromal cell-derived factors in modulating B cell function in SLE.
  • To identify specific molecular mechanisms linking the microenvironment to B cell autoreactivity in lupus.

Main Methods:

  • Analysis of immune cell microenvironment in human and murine lupus models.
  • Metabolomic profiling of B cells.
  • Assessment of B cell autoreactivity and disease markers.

Main Results:

  • Splenic stromal cells produce acetylcholine.
  • Acetylcholine induces a metabolic switch in B cells towards fatty acid oxidation.
  • Enhanced fatty acid oxidation in B cells correlates with increased autoreactivity and disease severity.

Conclusions:

  • Splenic stromal cell-derived acetylcholine is a key mediator in lupus pathogenesis.
  • Targeting acetylcholine or B cell metabolism may offer novel therapeutic strategies for SLE.