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Related Concept Videos

Autoimmune Disorders01:29

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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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Hypersensitivity Reactions: Immune-Complex Reactions01:19

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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
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Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Siglec-H protects from virus-triggered severe systemic autoimmunity.

Heike Schmitt1, Sabrina Sell2, Julia Koch1

  • 1Division of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91054 Erlangen, Germany.

The Journal of Experimental Medicine
|July 6, 2016
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Siglec-H normally regulates type I interferon (IFN) production by plasmacytoid dendritic cells (pDCs) during viral infections. Its absence leads to excessive IFN-α, triggering lupus-like autoimmune disease after cytomegalovirus infection.

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Area of Science:

  • Immunology
  • Virology
  • Autoimmunity

Background:

  • The link between viral infections and autoimmune diseases is debated.
  • Type I interferons (IFNs) are crucial for antiviral responses but also implicated in systemic lupus erythematosus (SLE) pathogenesis.
  • Plasmacytoid dendritic cells (pDCs) are primary producers of type I IFNs, with Siglec-H modulating their secretion.

Purpose of the Study:

  • To investigate the role of Siglec-H in modulating type I IFN production by pDCs.
  • To determine if Siglec-H deficiency influences autoimmune disease development following viral infection.

Main Methods:

  • Studied type I IFN-α production in vitro from Siglec-H-deficient pDCs.
  • Administered murine cytomegalovirus (mCMV) to Siglec-H knockout (KO) and wild-type mice.
  • Monitored viral replication, IFN-α levels, and development of autoimmune disease in KO and wild-type mice.

Main Results:

  • Siglec-H-deficient pDCs produced higher levels of IFN-α in vitro.
  • Siglec-H KO mice exhibited elevated IFN-α post-mCMV infection without impaired viral control.
  • mCMV infection in Siglec-H KO mice induced severe lupus-like autoimmune disease, characterized by nephritis, dependent on type I IFN signaling.

Conclusions:

  • Siglec-H acts as a crucial modulator of type I IFN responses to persistent viral infections.
  • Siglec-H deficiency promotes the induction of systemic autoimmunity following viral challenge.
  • Siglec-H plays a protective role in preventing virus-induced autoimmune disease.