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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Updated: Apr 19, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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The autoantigen TRIM21 assembles proinflammatory immune complexes after lytic cell death.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Autoimmune Diseases

Background:

  • Sjögren's disease (SjD) involves inflammation and autoantibodies against intracellular proteins like TRIM21/Ro52.
  • TRIM21 is an E3 ubiquitin ligase that targets intracellular pathogens.
  • The mechanism of TRIM21 becoming an autoantigen in SjD is not fully understood.

Purpose of the Study:

  • To investigate the release and autoantigenic properties of TRIM21 in Sjögren's disease.
  • To elucidate the role of TRIM21 immune complexes in disease pathogenesis.

Main Methods:

  • Analysis of TRIM21 release during different cell death pathways (pyroptosis, necroptosis, apoptosis).
  • Characterization of immune complex formation involving TRIM21 and autoantibodies.
  • Investigation of TRIM21 immune complex uptake by macrophages and subsequent inflammatory responses.

Main Results:

  • TRIM21 is released upon lytic cell death (pyroptosis, necroptosis), but not apoptosis.
  • Released TRIM21 forms large immune complexes (ICs) with circulating immunoglobulins, particularly in SjD patients.
  • TRIM21 ICs are internalized by macrophages, promoting inflammation, antigen presentation, and metabolic shifts in high interferon conditions.

Conclusions:

  • TRIM21 release during lytic cell death contributes to its autoantigenicity in Sjögren's disease.
  • TRIM21 immune complexes perpetuate inflammation and antigen presentation, potentially leading to high immunogenicity.
  • TRIM21 may play a critical role in the chronic inflammatory cycle of Sjögren's disease.