Información del artículo
Resumen
El monofosfato de adenosina cíclico (AMPc) induce la activación de la proteína cinasa A, la cual regula negativamente la activación, la proliferación celular y la producción de IL-2, en células T. En células infectadas con el virus de inmunodeficiencia humana, el monofosfato de adenosina cíclico suprime la actividad de transcripción del promotor del virus y el paso del ADN viral del citoplasma al núcleo. El incremento del monofosfato de adenosina cíclico mediado por células T reguladoras CD4+, empleando la inyección de esta molécula en células blanco a través de las uniones comunicantes o empleando el eje CD39-CD73 para generar adenosina es utilizado para suprimir otras poblaciones celulares.
En esta revisión se propone que la modulación del monofosfato de adenosina cíclico por las células T reguladoras CD4+ podría tener un papel dual durante la evolución de la infección por el virus de inmunodeficiencia humana. Su papel benéfico se centraría principalmente en el control de la replicación viral y factores de transcripción, o evitando la infección de nuevas células blanco por disminución en la expresión de los receptores virales. Paradójicamente, la segunda posibilidad es que el aumento del monofosfato de adenosina cíclico podría tener un papel perjudicial, debido al efecto negativo sobre la proliferación, activación, respuesta citotóxica y en la producción de citocinas que se observa durante la infección viral.
Palabras clave:
AMP cíclico
VIH
células T
replicación viral
uniones comunicantes
adenosina
Abstract
Cyclic adenosine monophosphate induces the activation of protein kinase A, which negatively regulates activation, proliferation and IL-2 production in T cells. In cells infected with human immunodeficiency virus, cyclic adenosine monophosphate suppresses the transcriptional activity of long terminal repeats and the amount of viral DNA from the cytoplasm to the nucleus. The increase in cyclic adenosine monophosphate mediated by CD4+ regulatory T cells, using either the influx of this molecule in target cells through the GAP junctions or by CD39-CD73 to generate adenosine, is used by CD4+ regulatory T cells to suppress other cell populations. In this review, we suggest that modulation of cyclic adenosine monophosphate by CD4+ regulatory T cells may have a dual role during the evolution of human immunodeficiency virus infection. The beneficial role would be mainly focused on the control of viral replication and transcription factors to replicate the virus, and/or preventing the infection of new target cells, decreasing the expression of the viral co-receptors. Paradoxically to this beneficial role, the second possibility is that increased cyclic adenosine monophosphate could have a detrimental role, due to the negative effect on proliferation, activation, cytotoxic response and cytokine production, which occurs during viral infection.
Key words:
Cyclic AMP
HIV
T cells
virus replication
Gap junctions
adenosine
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