Mueller, Tonina T. and Pilartz, Mona and Thakur, Manovriti and Langheinrich, Torben and Luo, Junfu and Block, Rebecca and Hoeflinger, Jonathan K. L. and Meister, Sarah and Karaj, Flavio and Perez, Laura Garcia and Öllinger, Rupert and Engleitner, Thomas and Thoss, Jakob and Voelkl, Michael and Tersteeg, Claudia and Koedel, Uwe and Kohlmaier, Alexander Zigman and Teupser, Daniel and Wygrecka, Malgorzata and Ye, Haifeng and Preissner, Klaus T. and Radbruch, Helena and Elezkurtaj, Sefer and Mack, Matthias and von Hundelshausen, Philipp and Weber, Christian and Massberg, Steffen and Schulz, Christian and Rad, Roland and Huber, Samuel and Ishikawa-Ankerhold, Hellen and Engelmann, Bernd (2024) Mutual regulation of CD4+T cells and intravascular fibrin in infections. HAEMATOLOGICA, 109 (8). pp. 2487-2499. ISSN 0390-6078, 1592-8721
Full text not available from this repository. (Request a copy)Abstract
Innate myeloid cells especially neutrophils and their extracellular traps are known to promote intravascular coagulation and thrombosis formation in infections and various other conditions. Innate myeloid cell-dependent fibrin formation can support systemic immunity while its dysregulation enhances the severity of infectious diseases. Less is known about the immune mechanisms preventing dysregulation of fibrin homeostasis in infection. During experimental systemic infections local fibrin deposits in the liver microcirculation cause rapid arrest of CD4+ + T cells. Arrested T-helper cells mostly represent Th17 cells that partially originate from the small intestine. Intravascular fibrin deposits activate mouse and human CD4+ + T cells which can be mediated by direct fibrin-CD4+ + T-cell interactions. Activated CD4+ + T cells suppress fibrin deposition and microvascular thrombosis by directly counteracting coagulation activation by neutrophils and classical monocytes. T-cell activation, which is initially triggered by IL-12p40- and MHC-II-dependent mechanisms, enhances intravascular fibrinolysis via LFA-1. Moreover, CD4+ + T cells disfavor the association of the thrombin-activatable fibrinolysis inhibitor (TAFI) with fibrin whereby fibrin deposition is increased by TAFI in the absence but not in the presence of T cells. In human infections thrombosis development inversely related to microvascular levels of CD4+ + T cells. Thus, fibrin promotes LFA-1-dependent T-helper cell activation infections which drives a negative feedback cycle that rapidly restricts intravascular fibrin and thrombosis development.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | IMMUNE-RESPONSE; COAGULATION; THROMBIN; ROLES; SEPSIS; TAFI |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 27 Jan 2026 07:22 |
| Last Modified: | 27 Jan 2026 07:22 |
| URI: | https://pred.uni-regensburg.de/id/eprint/65341 |
Actions (login required)
 |
View Item |
