Mechanism by which immune complexes are deposited in hosts tissue

Isaac Ginsburg, Mark Feldman

Research output: Contribution to journalComment/debate

Abstract

We offer an explanation how immune complexes are deposited in tissues of auto-immune disorders in humans. These disorders are characterized by the accumulation in tissues of large numbers of neutrophils, which can shed out long extracellular traps (NETs) rich in a nucleosome and in highly opsonic poly cations, histone, LL37, defensins and elastase possessing properties similar to antibodies. These can bind by strong electrostatic forces to negatively charged domains in immune globulins, thus facilitating their deposition and internalization by tissue cells. However, the main cause for tissue damage in auto-immune patients is inflicted by the plethora of toxic pro-inflammatory agents released by activated neutrophils. To ameliorate tissue damage and the cytokine storms, it is recommended to administer to patients highly anionic heparins accompanied by steroids, methotrexate, colchicine, copaxone, and also by additional agents which retarded neutrophil functions.

Original languageEnglish
Pages (from-to)349-351
Number of pages3
JournalInflammopharmacology
Volume30
Issue number1
DOIs
StatePublished - Feb 2022

Keywords

  • Auto-immune inflammatory disorders
  • Immune complexes
  • Pro-inflammatory agents

All Science Journal Classification (ASJC) codes

  • Pharmacology (medical)
  • Pharmacology
  • Immunology

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