<?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>2310-0265</journal-id>
<journal-title><![CDATA[Revista CON-CIENCIA]]></journal-title>
<abbrev-journal-title><![CDATA[Rev.Cs.Farm. y Bioq]]></abbrev-journal-title>
<issn>2310-0265</issn>
<publisher>
<publisher-name><![CDATA[Facultad de Ciencias Farmacéuticas y BioquímicasUniversidad Mayor de San Andrés]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2310-02652024000100003</article-id>
<article-id pub-id-type="doi">10.53287/entk9814iz47c</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Polimorfismo+49 (A/G) en el exón 1 del gen CTLA-4 y la susceptibilidad a Lupus Eritematoso Sistémico en población boliviana]]></article-title>
<article-title xml:lang="en"><![CDATA[Polymorphism in the CTLA-4 exon 1 +49(A/G) and its susceptibility to Systemic Lupus Erythematosus in the Bolivian population]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Barreto Chávez]]></surname>
<given-names><![CDATA[Claudia Cecilia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Guerra Monrroy]]></surname>
<given-names><![CDATA[Gabriela Carola]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Tordoya]]></surname>
<given-names><![CDATA[Luis Fernando Sosa]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,aff1  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<aff id="Af2">
<institution><![CDATA[,aff2  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>06</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>06</month>
<year>2024</year>
</pub-date>
<volume>12</volume>
<numero>1</numero>
<fpage>3</fpage>
<lpage>15</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.bo/scielo.php?script=sci_arttext&amp;pid=S2310-02652024000100003&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.bo/scielo.php?script=sci_abstract&amp;pid=S2310-02652024000100003&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.bo/scielo.php?script=sci_pdf&amp;pid=S2310-02652024000100003&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción. Lupus eritematoso sistémico (LES), es una enfermedad autoinmune sistémica que afecta a diferentes órganos y sistemas, se presenta principalmente en mujeres en edad fértil. Entre los factores predisponentes, los genéticos juegan un rol importante en la predisposición al desarrollo de la enfermedad. El Antígeno 4 del linfocito T citotóxico (CTLA-4) es un receptor de superficie celular perteneciente a la familia de la molécula estimuladora CD28 y es un receptor implicado en la regulación negativa de los linfocitos T. El polimorfismo +49 (A/G) del gen CTLA-4 ha sido asociado como factor de susceptibilidad genética a LES.  Objetivo. Determinar la asociación genética entre el polimorfismo genético y alélico de +49 (A/G) del gen CTLA-4 con susceptibilidad a LES y sus manifestaciones clínicas en población boliviana  Materiales y métodos. Se incluyó 80 pacientes lúpicos y 80 pacientes sin la enfermedad (grupo control) quienes asistieron al Instituto SELADIS de la ciudad de La Paz. El genotipado se realizó mediante la reacción en cadena de la polimerasa y fragmentos de restricción de longitud polimórfica (PCR-RFLP), los productos amplificados fueron revelados mediante de electroforesis en gel de agarosa.  Resultados. El estudio muestra que el genotipo G/G (OR=3.33, p=0.01) y el Alelo G (OR=1.79, p=0.02) del CTLA-4, predisponen a un riesgo de desarrollo de LES. Se observó también que el genotipo A/A y Alelo A predisponen a fotosensibilidad (OR=4.73, p=0.002), el genotipo A/G predispone a complicaciones renales (OR=7.41, p=0.0001), serositis (OR=4.94, p=0.02) y hematológicas (OR=3.2, p=0.02), el alelo G es factor de riesgo para desarrollo de manifestaciones articulares (OR= 2.35, p=0.01) y hematológicas (OR= 2.35, p=0.01).  Conclusiones. La presencia del alelo G y del genotipo G/G en la posición +49 del exón 1 del gen CTLA-4 demuestra ser factor de susceptibilidad al desarrollo de LES y algunas de sus manifestaciones clínicas en población boliviana.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Introduction. Systemic lupus erythematous (SLE) is a systemic autoimmune disease that affects different organs and systems occurs mainly in women of childbearing age. Among the predisposing factors, the genetic-related play an important role predisposing the development of this disease. Cytotoxic T lymphocyte Antigen 4 (CTLA-4) is a cell surface receptor belonging to the CD28 stimulatory molecule family, CTLA-4 is a receptor involved in the negative regulation of T lymphocytes. The polymorphism +49 (A/G) in the CTLA-4 gene has been associated as a genetic factor of susceptibility to SLE.  Objective. To determine the association between the genetic and allelic polymorphism of + 49 (A/G) CTLA-4 gene with the susceptibility to SLE and its clinical manifestations in the Bolivian population.  Materials and methods. 160 patients were selected to the study, 80 SLE affected patients and 80 patients without SLE (control group). Genotyping was identified by Polymerase Chain Reaction and Restriction Fragment Length Polymorphism (PCR-RFLP), the amplified products were visualized by agarose gel electrophoresis.  Results.  The study showed that the G/G genotype (OR=3.33, p&lt;0.05) and the G Allele (OR=1.79, p&lt;0.05) of CTLA-4 are associated to an increasing risk to develop SLE. It was also observed that the A/A genotype and A allele predisposed to photosensitivity susceptibility (OR=4.73, p&lt;0.05), the A/G genotype predisposes to renal complications (OR=7.41, p&lt;0.05), serositis (OR= 4.94, p&lt;0.05) and haematological complications (OR=3.2, p&lt;0.05), while the G allele is a risk factor for the development of joint manifestations (OR= 2.35, p&lt;0.05) and haematological manifestations (OR= 2.35, p&lt;0.05).  Conclusion. The presence of the G allele and the G/G genotype at position +49 of exon 1 of the CTLA-4 gene proved to be a susceptibility factor for the development of SLE and some of its clinical manifestations in the Bolivian population.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Lupus Eritematoso Sistémico]]></kwd>
<kwd lng="es"><![CDATA[CTLA-4]]></kwd>
<kwd lng="es"><![CDATA[asociación genética]]></kwd>
<kwd lng="es"><![CDATA[polimorfismo genético]]></kwd>
<kwd lng="en"><![CDATA[Systemic Lupus Erythematosus]]></kwd>
<kwd lng="en"><![CDATA[CTLA-4 gene]]></kwd>
<kwd lng="en"><![CDATA[genetic association]]></kwd>
<kwd lng="en"><![CDATA[genetic polymorphism]]></kwd>
</kwd-group>
</article-meta>
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