Mediators of Inflammation and Their Effect on Resident Renal Cells: Implications in Lupus Nephritis

Table 1

Mediators of inflammation that play important roles in the pathogenesis of lupus nephritis.

Inflammatory mediator	Putative roles in lupus nephritis
IL-6	(i) Activates B cells
	(ii) Induces glomerulonephritis
IFN-𝛼	(i) Interferes with vascular repair by inducing endothelial progenitor cell apoptosis
	(ii) Induces renal dysfunction, glomerulonephritis, crescent formation, and tubulointerstitial nephritis
IFN-𝛾	Promotes macrophage recruitment into the kidney and the development of glomerulonephritis
TNF-𝛼	(i) Regulates physiological and inflammatory immune responses
	(ii) Induces synthesis of IL-1𝛽 and IL-6 in mesangial cells and proximal renal tubular epithelial cells
	(iii) Elicits both proinflammatory and anti-inflammatory actions in lupus nephritis
Hyaluronan (HA)	(i) Forms HA cables that can prevent leukocyte adhesion to their receptors
	(ii) Induces chemokine secretion
	(iii) Possesses proinflammatory and anti-inflammatory properties