Immunmodulation der Endometriose

In: Der Gynäkologe · 2002 · vol. 35(3) , pp. 238–242 · doi:10.1007/s00129-002-1177-5 · W1582527684
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VEGF-A, RANTES, and Eotaxin are implicated in endometriosis progression, vascularization, and infertility through inflammatory cell recruitment and activation.

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This paper reviews molecular mechanisms relevant to endometriosis, focusing on how immunomodulation and angiogenesis may drive disease progression. It highlights VEGF-A as an angiogenic mediator involved in cycle-dependent vascularization in normal endometrium and in vascularization of endometriotic lesions, and it discusses chemokines RANTES and eotaxin as factors produced in endometrium and endometriosis tissue that recruit and activate inflammatory cells such as monocytes/activated T cells and eosinophils, potentially contributing to pain and infertility. A key caveat is that the work is a narrative summary of existing mechanistic links rather than presenting new experimental data or quantifying causal effects. This paper is centrally about endometriosis — specifically, immunomodulation via VEGF-A, RANTES, and eotaxin and their potential roles in inflammation, angiogenesis, and symptom-related progression.

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Zusammenfassung Neue Diagnostik- und Therapieansätze der Endometriose setzen das Verständnis der molekularen Pathomechanismen voraus. Die Aktivierung der Angiogenese scheint – auch über lokal im Gewebe exprimierte Entzündungsmediatoren – relevant für die Progression der Erkrankung zu sein. Damit könnten diese Faktoren als molekulare Marker für die Aktivität der Erkrankung dienen. Der spezifische Angiogenesemediator VEGF-A (VEGF: vascular endothelial growth factor) ist offensichtlich an der zyklusabhängigen Regulation der Vaskularisierung im normalen Endometrium und bei der Gefäßneubildung von Endometrioseherden beteiligt. RANTES (Regulated upon Activation, normal T-cell-Expressed and Secreted) und Eotaxin sind spezifische Chemokine für Monozyten und aktivierte T-Zellen bzw. eosinophile Granulozyten. Diese Chemokine werden im Endometrium- und Endometriosegewebe gebildet und könnten im Rahmen der Makrophagenaktivierung und Rekrutierung von Entzündungsmediatoren eine Rolle bei der endometrioseassoziierten Infertilität und Beschwerdesymptomatik spielen und zur Progression der Erkrankung beitragen. Abstract Novel approaches for diagnosis and therapy of endometriosis require a more detailed understanding of the molecular pathomechanisms of the disease. The progression of endometriosis seems to be associated with activation of angiogenesis which could also be mediated by the local expression of chemokines. VEGF-A (VEGF: vascular endothelial growth factor) seems to be involved in the menstrual cycle-dependent regulation of vascularisation in normal endometrium and endometriotic implants. RANTES (Regulated upon Activation, normal T-cell-Expressed and Secreted) and Eotaxin are specific chemokines for monocytes and activated T-cells or eosinophil granulocytes, respectively. These chemokines are expressed in normal endometrium and endometriosis tissue and might contribute to endometriosis-associated infertility and pain by recruitment and activation of makrophages and other inflammatory cells. Since inflammatory cells are also a rich source of angiogenetic factors, the progression of the disease would be promoted. Similar content being viewed by others Author information Authors and Affiliations Rights and permissions About this article Cite this article Greb, R., Löbbecke, K., Paletta, J. et al. Immunmodulation der Endometriose. Gynäkologe 35, 238–242 (2002). https://doi.org/10.1007/s00129-002-1177-5 Published: Issue date: DOI: https://doi.org/10.1007/s00129-002-1177-5

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