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Expansión de las células Treg asociadas al tumor tras la interrupción de un circuito de retroalimentación dependiente
Francesco Marangoni1, Ademi Zhakyp2, Michela Corsini3
1The Center for Immunology and Inflammatory Diseases (CIID), Massachusetts General Hospital, Boston, MA 02114, USA; Harvard Medical School, Boston, MA 02115, USA; Department of Physiology and Biophysics, University of California, Irvine, Irvine, CA 92697, USA; Institute for Immunology, University of California, Irvine, Irvine, CA 92697, USA.
Cell
|June 22, 2021
Resumen
Las células reguladoras de Foxp3+ T (Treg) controlan la tolerancia tumoral mediante la interacción con las células dendríticas (cDC). Las células Treg utilizan CTLA-4 para limitar su propia activación, un proceso crucial para el rechazo tumoral.
Área de la Ciencia:
- Inmunología
- Biología del cáncer
- Interacciones celulares
Sus antecedentes:
- Las células reguladoras de Foxp3+ T (Treg) son cruciales para mantener la tolerancia inmunológica en el microambiente tumoral (TME).
- Los mecanismos precisos que regulan la función y la activación de las células Treg dentro de la EMT no se comprenden completamente.
Objetivo del estudio:
- Investigar las interacciones celulares que rigen la activación y la función de las células Treg dentro de la EMT.
- Para aclarar los circuitos de retroalimentación reguladores que controlan el número y la actividad de las células Treg en los tumores.
Principales métodos:
- Se empleó microscopía intravital para visualizar y analizar las interacciones celulares en tiempo real dentro de la EMT.
- Caracterización del reconocimiento de células Treg de antígenos presentados por células dendríticas convencionales asociadas al tumor (cDC).
- Evaluación del papel de CTLA-4 y CD28 en la regulación y proliferación de las células Treg.
Principales resultados:
- Las células Treg reconocen preferentemente los antígenos presentados por los CDC en la EMT.
- Las interacciones inestables con los CDC mantienen la función de las células Treg, mientras que las interacciones estables activan las células T auxiliares.
- Las células Treg utilizan CTLA-4 para regular a la baja las moléculas coestimulantes en las CDC, limitando su propia activación.
- El bloqueo de CTLA-4 conduce a la hiperproliferación de las células Treg, lo que requiere la inactivación de las células Treg para el rechazo tumoral.
Conclusiones:
- Las células Treg autorregulan su tamaño de población en el TME a través de un bucle de retroalimentación dependiente de CTLA-4 y CD28.
- La interrupción de este bucle regulador de células Treg por el bloqueo de CTLA-4 puede contrarrestar la eficacia terapéutica en el tratamiento del cáncer.
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