Transcriptional Control of Inflammatory Responses (original) (raw)

  1. Gioacchino Natoli2
  2. 1Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, California 90095
  3. 2Department of Experimental Oncology, European Institute of Oncology (IEO), I-20139 Milan, Italy
  4. Correspondence: gioacchino.natoli{at}ieo.eu

Abstract

The inflammatory response requires the activation of a complex transcriptional program that is both cell-type- and stimulus-specific and involves the dynamic regulation of hundreds of genes. In the context of an inflamed tissue, extensive changes in gene expression occur in both parenchymal cells and infiltrating cells of the immune system. Recently, basic transcriptional mechanisms that control inflammation have been clarified at a genome scale, particularly in macrophages and conventional dendritic cells. The regulatory logic of distinct groups of inflammatory genes can be explained to some extent by identifiable sequence-encoded features of their chromatin organization, which impact on transcription factor (TF) accessibility and impose different requirements for gene activation. Moreover, it has become apparent that the interplay between TFs activated by inflammatory stimuli and master regulators exerts a crucial role in controlling cell-type-specific transcriptional outputs.