AI Article Synopsis
- - The text describes how immune complexes accumulate in tissues during autoimmune disorders, highlighting the role of neutrophils that release extracellular traps (NETs) with properties resembling antibodies.
- - Neutrophils release toxic inflammatory substances that contribute significantly to tissue damage in autoimmune patients, despite their role in binding immune globulins.
- - To reduce tissue damage and inflammatory responses, the text suggests treating patients with highly anionic heparins alongside medications such as steroids, methotrexate, and colchicine to inhibit neutrophil activity.
Article 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.
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| http://dx.doi.org/10.1007/s10787-021-00910-y | DOI Listing |
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