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HYPOTHESIS AND THEORY article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1404161
Interplay of trauma-triggered auto-inflammation and T-cell auto-reactivity in posttraumatic dystrophy
Provisionally accepted- Dietrich Bonhoeffer Klinikum, Neubrandenburg, Germany
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Damage-associated molecular patterns (DAMPs) cause sterile autoinflammation after a traumatic incident in human tissues via innate immunity. The auto-reactivity of natural killer T cells (NK-T cells)[P1] instigated by DAMPactivated exocytosis of dendritic cell (DC) vesicles forces implementation of T helper cells, which aggravate inflammatory reactions such as AV [P2]shunts and hyperperfusion of the ROI[P3] with hypoxia of capillaries. For example, in trauma patients, elevated venous pO 2 [P4] was found compared to that in the contralateral extremity of > 20 mmHg 2.66 kPa[P5]. Scintigraphic perfusion of the ROI showed elevated values of over 90 % on average compared with the healthy side. These findings suggest local capillary stasis, hypoxia, and acidosis. In the initial process, macrophages and dendritic cells play an important role, along with DAMPs, in the activation of innate immunity. Additional tissue-homing NKT cells are activated by releasing pro-inflammatory cytokines. The resulting "cytokinestorm" opens options for perpetuation by diverse autocrine loops and inflammasomes. Finally, antibodies against self-molecules are directed against cells and tissues. In a biological sense, this represents the worst scenario in chronic-aseptic inflammatory reactions after trauma and must be fought from the beginning to avoid chronification and spreading, which can lead to fibrosis and functional impairment of the injured extremity. This is the feared endpoint of posttraumatic dystrophy.
Keywords: damage-associated molecular pattern, innate immunity, Autoreactivity, NKT cell, AV-shunt, Hyperperfusion, hypoxia, posttraumatic dystrophy 1 Introduction
Received: 20 Mar 2024; Accepted: 15 Apr 2025.
Copyright: © 2025 Scola. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Egmont Scola, Dietrich Bonhoeffer Klinikum, Neubrandenburg, Germany
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