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This video by Dr. Sarah Zielsdorf, MD, MS delves into the complex immunology of adenomyosis and endometriosis, drawing from a 1998 Human Reproduction Update review. It highlights immune system dysfunction as a core element, detailing the cascade of cellular and humoral immunity changes. The discussion emphasizes the prevalence of autoantibodies, such as PI-G, and their potential link to infertility and reproductive challenges in affected individuals.
Dr. Sarah Zielsdorf, MD, MS:
immune dysregulation really is the key. This paper which was a review in human reproduction update was from 1998 and it really discusses the fact that adinomiiosis as known at that time is a disease state of one that is of immune system dysfunction.
Again, adenomiiosis is characterized as ectopic endometrial tissue within the myometrium in the uterus. The only difference between adenomiosis and endometriosis is the sight of endometriotic tissues inside or outside of the uterus. It is well known that endometriosis is frequently associated with various autoimmune phenomena. This short review highlighted covers various aspects of the immune cascade found in adenomiosis. In adenomiosis, a series of immune responses is activated including changes in both cellular and humoral immunity. This means that there is a strong expression of cell surface antigens or adhesion molecules. an increased number of cells of the immune system including macrofasages and deposition of imunoglobulins and compliment components which help to bind toxins and an and uh pathogens. Furthermore, the disease exhibits exhibits high frequency of auto antibodies in the peripheral blood. Thus an imunological vicious circle is formed in the endometrium in adenomiosis. Endometrial cells seem to be under imunological stress protecting themselves by exposing health shock health shock proteins. It is concluded that the endometrial environment in adenomiosis differs widely from that in normal fertile women. These abnormal immune responses might be involved in poor reproductive performance in adinomiiosis and trending toward infertility. This figure we can see the incidence of different types of auto antibodies in patients with adenomiosis. These include anti-cardiolypin antibodies both IgM and IgG antiphospatitic acid anti-IGG antibbody antifphosphotidal serereine IGG antibbody antifphosphotidal glycerol IGG antibbody and anti-phosphidal enosl IGG antibbody and these are and these are targets on uh surfaces of um membranes and these are highly correlated with different autoimmune diseases.
I know this is highly technical but I want to drive home the point that we know a lot about the immunology and the pathogenesis of endometriosis. And this is a nice review paper on this.
Endometriosis forms a specific hormonal environment. It's characterized by high concentrations of estrogens and androgens whose levels are several times greater than those found in patients peripheral blood. Consequently, different phenomena are triggered including cell proliferation and release of various imunological and inflammatory factors. There is systemic immune system reactivation, excuse me, systemic immune reactions. This includes non-specific markers including CA125 but also spec more specific markers like C reactive protein a marker of chronic inflammation and anti-uclear antibbody which is a precursor in many cases for autoimmune conditions. It is a chronic inflammatory disorder. you're going to have the development of and release of pro-inflammatory cytoines including TNF alpha, IL1, IL6, IL8, IL10, TGF beta 1. You're going to have infiltration of lymphosytes or lymphosetic infiltration into tissues which is a hallmark of autoimmune disease. icosenoid which are fatty acids and metalloprotein protein synthesis activation of polyclonal belymphosytes and abnormalities of T and Bymphosytes which plays a role in why things like lodone would be important for use impaired aptosis or programmed cell killing disturbed localization of T- regulatory cells which are the traffic cops of the cell traffic cops of the system and abnormal maturation of natural killer cells. Within endometriotic lesions, there's localized hypoxia or lack of oxygenation, lack of blood flow. There is scarring within these lesions. Therefore we get increase in active angioenesis or factors that help to increase um blood vessel formation including veg f alpha interlucan 6 IL8 and increasing TGF beta and IL10 and that decreases the ability of natural killer cells to do their job and it also impairs the regulation of macrofase function. There is a potential correlation and definite coexistence with other autoimmune diseases.
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