دورية أكاديمية
Mutual regulation of CD4+ T cells and intravascular fibrin in infections
| العنوان: | Mutual regulation of CD4+ T cells and intravascular fibrin in infections |
|---|---|
| المؤلفون: | Tonina T. Mueller, Mona Pilartz, Manovriti Thakur, Torben LangHeinrich, Junfu Luo, Rebecca Block, Jonathan K.L. Hoeflinger, Sarah Meister, Flavio Karaj, Laura Garcia Perez, Rupert Öllinger, Thomas Engleitner, Jakob Thoss, Michael Voelkl, Claudia Tersteeg, Uwe Koedel, Alexander Zigman Kohlmaier, Daniel Teupser, Malgorzata Wygrecka, Haifeng Ye, Klaus T. Preissner, Helena Radbruch, Sefer Elezkurtaj, Matthias Mack, Philipp von Hundelshausen, Christian Weber, Steffen Massberg, Christian Schulz, Roland Rad, Samuel Huber, Hellen Ishikawa-Ankerhold, Bernd Engelmann |
| المصدر: | Haematologica, Vol 999, Iss 1 (2024) |
| بيانات النشر: | Ferrata Storti Foundation, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Diseases of the blood and blood-forming organs |
| مصطلحات موضوعية: | Diseases of the blood and blood-forming organs, RC633-647.5 |
| الوصف: | 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 fibrinolysis inhibitor TAFI with fibrin whereby fibrin deposition is increased by TAFI in the absence but not presence of T cells. In human infections thrombosis development is inversely related to microvascular levels of CD4+ T cells. Thus, fibrin promotes LFA-1 dependent T helper cell activation in infections which drives a negative feedback cycle that rapidly restricts intravascular fibrin and thrombosis development. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 0390-6078 1592-8721 |
| العلاقة: | https://haematologica.org/article/view/11539Test; https://doaj.org/toc/0390-6078Test; https://doaj.org/toc/1592-8721Test |
| DOI: | 10.3324/haematol.2023.284619 |
| الوصول الحر: | https://doaj.org/article/4839f9e3a00e42f59cb668d05a73ce41Test |
| رقم الانضمام: | edsdoj.4839f9e3a00e42f59cb668d05a73ce41 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 03906078 15928721 |
|---|---|
| DOI: | 10.3324/haematol.2023.284619 |