<?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>1665-1146</journal-id>
<journal-title><![CDATA[Boletín médico del Hospital Infantil de México]]></journal-title>
<abbrev-journal-title><![CDATA[Bol. Med. Hosp. Infant. Mex.]]></abbrev-journal-title>
<issn>1665-1146</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Salud, Hospital Infantil de México Federico Gómez]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1665-11462025000400001</article-id>
<article-id pub-id-type="doi">10.24875/bmhim.24000174</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Inmunoterapias y su capacidad de preservar células beta en la diabetes tipo 1: una revisión de la inmunoterapia actual]]></article-title>
<article-title xml:lang="en"><![CDATA[Immunotherapies and their potential to preserve beta cells in type 1 diabetes: a review of current immunotherapy]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Bonilla-Bonilla]]></surname>
<given-names><![CDATA[Juan D.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Chávez-Sánchez]]></surname>
<given-names><![CDATA[Luis]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Legorreta-Haquet]]></surname>
<given-names><![CDATA[María V.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto Politécnico Nacional Escuela Superior de Medicina ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Instituto Mexicano del Seguro Social Unidad Médica de Alta Especialidad y Hospital de Pediatría ]]></institution>
<addr-line><![CDATA[Ciudad de México ]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>08</month>
<year>2025</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>08</month>
<year>2025</year>
</pub-date>
<volume>82</volume>
<numero>4</numero>
<fpage>203</fpage>
<lpage>218</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1665-11462025000400001&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1665-11462025000400001&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1665-11462025000400001&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La diabetes tipo 1 es una enfermedad crónica de origen inmunitario que provoca la pérdida de células beta en el páncreas, caracterizada clínicamente por polidipsia, polifagia y pérdida de peso. La enfermedad es más frecuente en la primera y la segunda décadas de la vida, con un aumento anual constante. La dependencia de la terapia con insulina de forma indefinida es bien conocida. Aunque los avances en esta área, como los nuevos dispositivos de monitorización continua de la glucosa con infusión subcutánea continua de insulina, han mejorado la calidad de vida de los pacientes, no afectan a la patogénesis de la enfermedad y no reducen de forma constante las complicaciones a largo plazo. Además de exigir sacrificios en el estilo de vida y, en muchos casos, no alcanzar los puntos terapéuticos objetivo, aumenta el riesgo de hipoglucemia, una complicación aguda y potencialmente mortal. Tras décadas de investigación y avances en tecnologías terapéuticas, se han desarrollado enfoques basados en diversos mecanismos de la patogénesis de la enfermedad. Esta revisión se centra en nuevos enfoques de inmunoterapia para la diabetes tipo 1, incluidas las terapias dirigidas a células, las citocinas y los trasplantes de células para preservar la función de las células beta.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Type 1 diabetes is a chronic immune-mediated disease that leads to the loss of beta cells in the pancreas, clinically characterized by polydipsia, polyphagia, and weight loss. The disease is most prevalent in the first and second decades of life, with a consistent annual increase. The dependence on insulin therapy indefinitely is well known. Although advances in this area, such as new continuous glucose monitoring devices with continuous subcutaneous insulin infusion, have improved patient quality of life, they do not affect disease pathogenesis and do not consistently reduce long-term complications. In addition to requiring lifestyle sacrifices and, in many cases, failing to meet therapeutic target points, it increases the risk of hypoglycemia, an acute and potentially fatal complication. Following decades of research and advances in therapeutic technologies, approaches have been developed based on diverse mechanisms in the disease's pathogenesis. This review focuses on new immunotherapy approaches for type 1 diabetes, including cell-targeted therapies, cytokines, and cell transplants to preserve beta-cell function.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Diabetes mellitus tipo 1]]></kwd>
<kwd lng="es"><![CDATA[Teplizumab]]></kwd>
<kwd lng="es"><![CDATA[Rituximab]]></kwd>
<kwd lng="es"><![CDATA[Anticuerpos]]></kwd>
<kwd lng="es"><![CDATA[Inmunoterapia]]></kwd>
<kwd lng="es"><![CDATA[Células beta]]></kwd>
<kwd lng="en"><![CDATA[Type 1 diabetes mellitus]]></kwd>
<kwd lng="en"><![CDATA[Teplizumab]]></kwd>
<kwd lng="en"><![CDATA[Rituximab]]></kwd>
<kwd lng="en"><![CDATA[Antibodies]]></kwd>
<kwd lng="en"><![CDATA[Immunotherapy]]></kwd>
<kwd lng="en"><![CDATA[Beta cells]]></kwd>
</kwd-group>
</article-meta>
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