The Local Immune Mechanisms Involved in the Formation of Endometriotic Lesions

Yulia S. Antsiferova, Natalya Sotnikov
In: Endometriosis - Basic Concepts and Current Research Trends · 2012 · doi:10.5772/29965 · W1577826334
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This paper explores the role of the immune system in the growth of ectopic endometrial-like tissue characteristic of endometriosis, viewing the condition as an autotransplant.

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This chapter reviews the complex interactions between immune cells and endometriotic tissue, focusing on how local immune mechanisms facilitate lesion formation. It details the roles of macrophages, natural killer cells, and T lymphocytes in promoting inflammation, angiogenesis, and survival of ectopic endometrial implants. The authors highlight that a state of chronic inflammation and impaired immune surveillance allows these lesions to establish themselves outside the uterine cavity. This paper is centrally about endometriosis — specifically examining the immunological pathways that drive the development and persistence of endometriotic lesions.

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Abstract

According to common view, endometriosis is characterized by the presence and growth of the endometrium-like glandular tissue and stroma outside the uterus. So, endometriosis would represent an autotransplant in which tissue is transplanted to an ectopic location in an organism. It is well known that the immune system plays the main role in regulation of tissue homeostasis in an organism. Thus, immunologists have a special interest in this disease as insights in the pathogenesis of endometriosis would help not only to understand how ectopic lesions grow but also allow searching new approaches to the medical treatment of this disease.
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Open access Submitted: 14 March 2011 Published: 09 May 2012 DOI: 10.5772/29965 From the Edited Volume Edited by Koel Chaudhury and Baidyanath Chakravarty Submitted: 14 March 2011 Published: 09 May 2012 © 2012 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Discover 2026 Nobel Laureate Francis Halzen’s chapter on IntechOpen >

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endometriosis

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