Making sense of IL-6 signalling cues in pathophysiology

FEBS Letters

article

David Millrine¹  Robert H. Jenkins¹  Stuart T. O. Hughes¹  Simon A. Jones¹ 

[1] Division of Infection & Immunity, School of Medicine, Cardiff University;Systems Immunity University Research Institute, Cardiff University

关键词: arthritis;    cytokine receptors;    cytokines;    epigenetics;    inflammation;    interleukin;    Jak-STAT signalling;    microRNA;    pathophysiology;    STAT transcription factors;   

DOI  :  10.1002/1873-3468.14201

来源: John Wiley & Sons Ltd.

【 摘 要 】

Unravelling the molecular mechanisms that account for functional pleiotropy is a major challenge for researchers in cytokine biology. Cytokine–receptor cross-reactivity and shared signalling pathways are considered primary drivers of cytokine pleiotropy. However, reports epitomized by studies of Jak-STAT cytokine signalling identify interesting biochemical and epigenetic determinants of transcription factor regulation that affect the delivery of signal-dependent cytokine responses. Here, a regulatory interplay between STAT transcription factors and their convergence to specific genomic enhancers support the fine-tuning of cytokine responses controlling host immunity, functional identity, and tissue homeostasis and repair. In this review, we provide an overview of the signalling networks that shape the way cells sense and interpret cytokine cues. With an emphasis on the biology of interleukin-6, we highlight the importance of these mechanisms to both physiological processes and pathophysiological outcomes.

【 授权许可】

Unknown