Non-inflammatory IFN

JUNB/AP-1 controls IFN-γ during inflammatory liver disease.

Understanding the molecular pathogenesis of inflammatory liver disease is essential to design efficient therapeutic approaches. In hepatocytes, the dimeric transcription factor c-JUN/AP-1 is a major mediator of cell survival during hepatitis, although functions for other JUN proteins in liver disease are less defined. Here, we found that JUNB was specifically expressed in human and murine immun...

Visceral perception: inflammatory and non-inflammatory mediators.

Visceral hypersensitivity is currently the most widely accepted mechanism responsible for abdominal pain. Inflammatory mediators are known to sensitise primary afferents and to recruit silent nociceptors. Recent evidence suggests that non-inflammatory mediators also have the potential to trigger visceral pain. This sequence of events may constitute part of an alerting system which prompts the c...

A single intradermal injection of IFN-γ induces an inflammatory state in both non-lesional psoriatic and healthy skin

Psoriasis is a chronic, debilitating, immune-mediated inflammatory skin disease. As IFN-γ is involved in many cellular processes, including activation of dendritic cells (DCs), antigen processing and presentation, cell adhesion and trafficking, and cytokine and chemokine production, IFN-γ-producing Th1 cells were proposed to be integral to the pathogenesis of psoriasis. Recently, IFN-γ was show...

IFN Signaling: How a Non-Canonical Model Led to the Development of IFN Mimetics

The classical model of cytokine signaling dominates our view of specific gene activation by cytokines such as the interferons (IFNs). The importance of the model extends beyond cytokines and applies to hormones such as growth hormone (GH) and insulin, and growth factors such as epidermal growth factor (EGF) and fibroblast growth factor (FGF). According to this model, ligand activates the cell v...

Non-steroidal anti-inflammatory drugs.