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Inmunidad del tipo T-helper 1 al trofoblasto en mujeres con abortos espontáneos recurrentes
J A Hill1, K Polgar, D J Anderson
1Fearing Research Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass 02115, USA.
JAMA
|June 28, 1995
Resumen
Las mujeres con aborto recurrente inexplicable (URA) muestran inmunidad del T-helper 1 (TH1) al trofoblasto, lo que puede causar insuficiencia reproductiva. Por el contrario, la inmunidad de tipo TH2 puede apoyar un embarazo exitoso.
Área de la Ciencia:
- Inmunología Inmunología.
- La Medicina Reproductiva es una de ellas.
- Biología celular Biología celular.
Sus antecedentes:
- El aborto recurrente inexplicable (ARI) afecta a numerosas mujeres, y sus fundamentos inmunológicos no se comprenden completamente.
- El papel de las respuestas inmunes, particularmente la diferenciación de las células T auxiliares, en el éxito o el fracaso del embarazo es un área crítica de investigación.
Objetivo del estudio:
- Investigar la hipótesis de que las células mononucleares de la sangre periférica en mujeres con URA producen citoquinas tipo T-helper 1 (TH1) en respuesta a los antígenos de los trofoblastos.
- Para diferenciar las respuestas inmunes en mujeres con ARU en comparación con controles reproductivamente normales.
Principales métodos:
- Un estudio de cohorte que involucró a 244 mujeres con ARU, 13 mujeres de control reproductivamente normales y 10 hombres.
- Las células mononucleares de la sangre periférica fueron estimuladas con antígenos de trofoblasto.
- Las supernatantes fueron evaluadas para efectos embriotóxicos en embriones de ratón y analizadas para perfiles de citoquinas (IFN-gamma, IL-2, TNF-beta, IL-4, IL-10, TNF-alfa) utilizando ELISA.
Principales resultados:
- Se detectó actividad embriotóxica en 160 de 244 pacientes con ARU, asociada significativamente con la presencia de interferón gamma (IFN-gamma).
- Los pacientes con ARU exhibieron citoquinas de tipo TH1 (TNF-alfa, TNF-beta) en respuesta a los antígenos de los trofoblastos.
- Los controles reproductivamente normales mostraron una embriotoxicidad mínima y predominantemente citoquinas de tipo TH2 (IL-10, IL-4), lo que sugiere una respuesta inmune protectora.
Conclusiones:
- La inmunidad de tipo TH1 dirigida contra los antígenos de los trofoblastos se asocia con la ARU y puede contribuir a la insuficiencia reproductiva.
- La inmunidad de tipo TH2 parece ser una respuesta natural y potencialmente beneficiosa al trofoblasto, que apoya un embarazo exitoso.
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