<?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>2448-9190</journal-id>
<journal-title><![CDATA[Revista alergia México]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. alerg. Méx.]]></abbrev-journal-title>
<issn>2448-9190</issn>
<publisher>
<publisher-name><![CDATA[Colegio Mexicano de Inmunología Clínica y Alergia A.C.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2448-91902020000400370</article-id>
<article-id pub-id-type="doi">10.29262/ram.v67i4.784</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Alteraciones inflamatorias clínicas y moleculares en enfermedad granulomatosa crónica]]></article-title>
<article-title xml:lang="en"><![CDATA[Clinical and molecular inflammatory alterations in chronic granulomatous disease]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[León-Lara]]></surname>
<given-names><![CDATA[Ximena]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rodríguez-D&#8217;Cid]]></surname>
<given-names><![CDATA[Roberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rioja-Valencia]]></surname>
<given-names><![CDATA[Ricardo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ayala-Alvirde]]></surname>
<given-names><![CDATA[Alexandra]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Aliaga-Taipe]]></surname>
<given-names><![CDATA[Ida Lizbeth]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Espinosa-Padilla]]></surname>
<given-names><![CDATA[Sara]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Blancas-Galicia]]></surname>
<given-names><![CDATA[Lizbeth]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Secretaría de Salud Instituto Nacional de Pediatría Unidad de Investigación en Inmunodeficiencias]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Instituto Nacional de Salud del Niño Laboratorio de Citometría de Flujo ]]></institution>
<addr-line><![CDATA[Lima ]]></addr-line>
<country>Perú</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2020</year>
</pub-date>
<volume>67</volume>
<numero>4</numero>
<fpage>370</fpage>
<lpage>380</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S2448-91902020000400370&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S2448-91902020000400370&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S2448-91902020000400370&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La enfermedad granulomatosa crónica (EGC) es un error innato de la inmunidad. Se caracteriza por deficiencia en la función del complejo de la NADPH oxidasa. La EGC ha sido una oportunidad para estudiar la función de las especies reactivas de oxígeno (ROS) en el sistema inmune innato. La ausencia de ROS producidas por la NADPH oxidasa en los neutrófilos y en los macrófagos lleva a mayor susceptibilidad a infecciones bacterianas y fúngicas, debido a que las ROS participan en la eliminación de los microorganismos. Las manifestaciones inflamatorias y autoinmunes también están presentes en la EGC, sin embargo, no es del todo clara la relación de causalidad entre la falta de ROS y los síntomas inflamatorios. Se han realizado diversos ensayos in vitro en humanos y experimentales en ratones para tratar de entender esta relación. Los estudios muestran que las ROS reaccionan con diferentes moléculas del sistema inmune, inhibiendo o estimulando su función, lo que explica que en la EGC se afecten varias vías de la inflamación que no están relacionadas entre sí; por lo tanto, han sido diversos los mecanismos de afectación descritos, como por ejemplo una mayor producción de citocinas proinflamatorias, un incremento en los linfocitos TH17 y una alteración en procesos como eferocitosis, apoptosis, autofagia e inflamasoma. El entendimiento de los mecanismos que llevan a la inflamación en la deficiencia del complejo de la NADPH oxidasa ha llevado a plantear nuevos tratamientos que actúan en procesos como la autofagia, el inflamosoma o el bloqueo de citocinas proinflamatorias. En esta revisión describimos las diferentes manifestaciones inflamatorias en EGC y los mecanismos moleculares a través de los cuales la falta de ROS conduce a la hiperinflamación.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Chronic granulomatous disease (CGD) is an inborn error of immunity. CGD is characterized by a deficiency in the function of the NADPH oxidase complex. CGD has been an opportunity to study the function of reactive oxygen species (ROS) in the innate immune system. The absence of ROS produced by NADPH oxidase in neutrophils and macrophages leads to an increased susceptibility to bacterial and fungal infections since ROS participate in the elimination of microorganisms. Inflammatory and autoimmune manifestations are also present in CGD; however, the causal connection between the lack of ROS and inflammatory symptoms is not entirely clear. Different in vitro assays have been conducted in humans and clinical trials have been conducted in mice in order to try to understand this relationship. Studies show that ROS react with different molecules of the immune system, either by inhibiting or by stimulating their function, which explains why various inflammation pathways that are not related to each other are affected in CGD; therefore, the described mechanisms of affectation have been diverse, such as a greater production of proinflammatory cytokines, an increase in TH17 lymphocytes, and an alteration in processes like spherocytosis, apoptosis, autophagy, and inflammosome. Understanding the mechanisms that lead to inflammation in the deficiency of the NADPH oxidase complex has led to the proposal of new treatments that act on processes like autophagy, inflammosome, or blocking proinflammatory cytokines. In this review, we describe the different inflammatory manifestations in CGD and the molecular mechanisms through which the lack of ROS leads to hyperinflammation.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[NADPH oxidasa]]></kwd>
<kwd lng="es"><![CDATA[Inflamación]]></kwd>
<kwd lng="es"><![CDATA[Enfermedad granulomatosa crónica]]></kwd>
<kwd lng="es"><![CDATA[Granulomas]]></kwd>
<kwd lng="es"><![CDATA[Especies reactivas de oxígeno]]></kwd>
<kwd lng="en"><![CDATA[NADPH oxidase]]></kwd>
<kwd lng="en"><![CDATA[Inflammation]]></kwd>
<kwd lng="en"><![CDATA[Chronic granulomatous disease]]></kwd>
<kwd lng="en"><![CDATA[Granulomas]]></kwd>
<kwd lng="en"><![CDATA[Reactive oxygen species]]></kwd>
</kwd-group>
</article-meta>
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