<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0300-9041</journal-id>
<journal-title><![CDATA[Ginecología y obstetricia de México]]></journal-title>
<abbrev-journal-title><![CDATA[Ginecol. obstet. Méx.]]></abbrev-journal-title>
<issn>0300-9041</issn>
<publisher>
<publisher-name><![CDATA[Federación Mexicana de Colegios de Obstetricia y Ginecología A.C.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0300-90412025001000447</article-id>
<article-id pub-id-type="doi">10.24245/gom.v93i10.197</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Inmunología, el fulcro de la endometriosis. Fisiopatología y blancos terapéuticos]]></article-title>
<article-title xml:lang="en"><![CDATA[Immunology, the fulcrum of endometriosis, physiopathology and therapeutic targets.]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ayala Yáñez]]></surname>
<given-names><![CDATA[Rodrigo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Soto Aburto]]></surname>
<given-names><![CDATA[Carlos Enrique]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Fuentes Astudillo]]></surname>
<given-names><![CDATA[Zomar Roberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Martínez Ruíz]]></surname>
<given-names><![CDATA[Mario]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Morales Velázquez]]></surname>
<given-names><![CDATA[Mario]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Centro Médico ABC  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Asociación Hispano Mexicana-CIMIGEN  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Hospital Ángeles México  ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2025</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2025</year>
</pub-date>
<volume>93</volume>
<numero>10</numero>
<fpage>447</fpage>
<lpage>462</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0300-90412025001000447&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0300-90412025001000447&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0300-90412025001000447&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  OBJETIVO: Analizar los mecanismos inmunológicos implicados en la fisiopatología de la endometriosis e identificar dianas terapéuticas emergentes para desarrollar tratamientos más precisos y efectivos.  METODOLOGÍA: Revisión de la bibliografía publicada del 2010 al 2024 en las bases de datos de PubMed y Google Académico con los términos MeSH específicos. Se seleccionaron artículos enfocados en los mecanismos inmunológicos, angiogénesis, respuesta hormonal y potencial de tratamiento de pacientes con endometriosis.  RESULTADOS: La endometriosis se caracteriza por una deficiencia en la regulación inmunológica multifactorial distinguida por citotoxicidad afectada por células NK debido a sobreexpresión de receptores inhibitorios (NKG2A, KIR2DL1, HLA-C2), predominio de macrófagos M2 con actividad angiogénica sobre M1 citotóxicos, disfunción de linfocitos T con perfil Th2 e incremento de células T reguladoras (Treg). Las lesiones endometriósicas evaden la apoptosis mediante exosomas inmunosupresores, activación aberrante del sistema del complemento (C3, C5), y modulación de receptores estrogénicos (ER&#945;, ER&#946;). La angiogénesis es promovida por el factor de crecimiento del endotelio vascular (VEGF) estimulado por la hipoxia (HIF-1&#945;), factores hormonales (aromatasa, SF1) e infiltrado inflamatorio. Las células dendríticas inmaduras participan en la neovascularización, en respuesta al factor de crecimiento del endotelio vascular. Se identificaron múltiples blancos terapéuticos: inhibidores del complemento (eculizumab, AMY-101), bloqueadores de TNF-&#945; (pentoxifilina, etanercept), moduladores de NK, terapias antiangiogénicas y probióticos.  CONCLUSIONES: Los mecanismos inmunológicos constituyen el fulcro fisiopatológico de la endometriosis. La inmunoterapia dirigida es una estrategia terapéutica prometedora que podría revolucionar el tratamiento de esta enfermedad compleja que afecta a millones de mujeres en el mundo.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  OBJECTIVE: To analyze the immunological mechanisms involved in the pathophysiology of endometriosis and to identify emerging therapeutic targets to develop more precise and effective treatments.  METHODOLOGY: A review of literature published from 2010 to 2024 was conducted using specific Medical Subject Headings (MeSH) terms in the PubMed and Google Scholar databases. Articles focusing on immunological mechanisms, angiogenesis, the hormonal response, and treatment potential in patients with endometriosis were selected.  RESULTS: Endometriosis is characterized by multifactorial immunological dysregulation, including impaired NK cell cytotoxicity due to the overexpression of inhibitory receptors (NKG2A, KIR2DL1, and HLA-C2); a predominance of M2 macrophages with angiogenic activity over M1 macrophages with cytotoxic activity; T-cell dysfunction with a Th2 profile; and an increase in regulatory T cells (Tregs). Endometriotic lesions evade apoptosis through the release of immunosuppressive exosomes, the aberrant activation of the complement system (C3 and C5), and the modulation of estrogen receptors (ER&#945; and ER&#946;). Angiogenesis is promoted by vascular endothelial growth factor (VEGF), which is stimulated by hypoxia (HIF-1&#945;), hormonal factors (aromatase and SF1), and an inflammatory infiltrate. Immature dendritic cells participate in neovascularization in response to VEGF. Several therapeutic targets have been identified, including complement inhibitors (eculizumab and AMY-101), TNF-&#945; blockers (pentoxifylline and etanercept), NK cell modulators, anti-angiogenic therapies, and probiotics.  CONCLUSIONS: Immunological mechanisms are the pathophysiological fulcrum of endometriosis. Targeted immunotherapy is a promising strategy that could transform the treatment of this complex disease affecting millions of women worldwide.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Endometriosis]]></kwd>
<kwd lng="es"><![CDATA[inmunología]]></kwd>
<kwd lng="es"><![CDATA[fisiopatología]]></kwd>
<kwd lng="es"><![CDATA[células NK]]></kwd>
<kwd lng="es"><![CDATA[macrófagos]]></kwd>
<kwd lng="es"><![CDATA[angiogénesis]]></kwd>
<kwd lng="es"><![CDATA[inmunoterapia]]></kwd>
<kwd lng="es"><![CDATA[sistema del complemento]]></kwd>
<kwd lng="en"><![CDATA[Endometriosis]]></kwd>
<kwd lng="en"><![CDATA[Immunology]]></kwd>
<kwd lng="en"><![CDATA[Pathophysiology]]></kwd>
<kwd lng="en"><![CDATA[NK cells]]></kwd>
<kwd lng="en"><![CDATA[Macrophages]]></kwd>
<kwd lng="en"><![CDATA[Angiogenesis]]></kwd>
<kwd lng="en"><![CDATA[Immunotherapy]]></kwd>
<kwd lng="en"><![CDATA[Complement system]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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