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Las células IgA+ inducidas por la inflamación desmantelan la inmunidad contra el cáncer de hígado
Shabnam Shalapour1, Xue-Jia Lin1,2, Ingmar N Bastian1
1Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, School of Medicine, University of California San Diego (UCSD), 9500 Gilman Drive, La Jolla, California 92093, USA.
Nature
|November 17, 2017
Resumen
La inflamación crónica en la enfermedad hepática grasa promueve el cáncer mediante el aumento de las células productoras de inmunoglobulina A (IgA+). Estas células suprimen los linfocitos T CD8+ citotóxicos, lo que dificulta la detección temprana del cáncer y promueve el crecimiento del tumor.
Área de la Ciencia:
- Inmunología
- Hepatología
- En el campo de la oncología
Sus antecedentes:
- El papel de la inmunidad adaptativa en el desarrollo temprano del cáncer sigue siendo objeto de debate.
- La enfermedad hepática grasa no alcohólica (EHGNA) está asociada con inflamación crónica y fibrosis.
- Las células productoras de inmunoglobulina A (IgA+) residentes en el hígado se acumulan en la EHGNA.
Objetivo del estudio:
- Investigar el papel de las células IgA+ en el desarrollo del carcinoma hepatocelular (CCH) en el contexto de la EHGNA.
- Esclarecer los mecanismos por los que las células IgA+ influyen en el microambiente tumoral y la vigilancia inmune.
Principales métodos:
- Análisis de tejidos hepáticos de modelos humanos y de ratones de EHGNA.
- Caracterización del fenotipo celular IgA+, incluida la expresión del ligando de muerte programada 1 (PD-L1) y la interleucina-10 (IL-10).
- Evaluación del impacto de las células IgA+ en la función citotóxica de los linfocitos T CD8+ y el desarrollo de HCC.
Principales resultados:
- Se observó una acumulación de células IgA+ que expresan PD-L1 e IL-10 en la EHGNA.
- Estas células IgA+ suprimían directamente los linfocitos T CD8+ citotóxicos del hígado.
- El agotamiento de las células T CD8+ aceleró el HCC, mientras que la inhibición de la generación de células IgA+ atenuó la carcinogénesis hepática y promovió la regresión del HCC.
Conclusiones:
- La supresión inducida por la inflamación de la activación citotóxica de los linfocitos T CD8+ por las células IgA+ es un mecanismo promotor de tumores en el CCH asociado a la NAFLD.
- La generación dirigida de células IgA+ ofrece una estrategia terapéutica potencial para el cáncer de hígado.
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