p50 NF- B and Dendritic Cells: a matter of life and death

Already 10 years ago, p50, a regulatory subunit of the NF- B family of transcription factors was shown to accumulate in the nucleus of LPS tolerant cells. More recently, the group of Antonio Sica has shown that accumulation of p50 homodimers in the nucleus of Tumour Associated Macrophages results in defective expression of proinflammatory cytokines (TNF- , IL-12) and reduced IL-10 production, correlating with increased tumour growth. Moreover, p50 accumulation in the nucleus of macrophages is an essential event for promoting endotoxin tolerance and pro-tumour polarized functions in these cells. Given the important role of p50 in controlling tolerance in innate immunity (macrophages), we wondered if p50 accumulation in Dendriic Cells could mediate their activation versus tolerant activity over adaptive immunity.

Autorentext

Paola Larghi was born in Milan in 1980, she got her degree in Biology at the University of Milan in 2005 and the PhD in Experimental Pathology in 2009. She worked at the European Institute of Oncology from 2003 to 2005 and at the Istituto Clinico Humanitas from 2006 to 2010. From 2010, she works at the Institut Curie in Paris.

Klappentext

Already 10 years ago, p50, a regulatory subunit of the NF- B family of transcription factors was shown to accumulate in the nucleus of LPS tolerant cells. More recently, the group of Antonio Sica has shown that accumulation of p50 homodimers in the nucleus of Tumour Associated Macrophages results in defective expression of proinflammatory cytokines (TNF- , IL-12) and reduced IL-10 production, correlating with increased tumour growth. Moreover, p50 accumulation in the nucleus of macrophages is an essential event for promoting endotoxin tolerance and pro-tumour polarized functions in these cells. Given the important role of p50 in controlling tolerance in innate immunity (macrophages), we wondered if p50 accumulation in Dendriic Cells could mediate their activation versus tolerant activity over adaptive immunity.