Table 2.

Immunopathology and possible immunopathogenesis of lupus nephritis

Tissue inflammation	Immunopathogenesis
Glomerulonephritis	Intrarenal IC deposition
	Circulating IC deposition
	In situ IC deposition
	Cytotoxic autoantibody-mediated damage
	Direct binding to autoantigens
	Charge–charge interactions between autoantibody and glomerular matrix
	Cellular autoimmunity elicited by
	Monocytes/macrophages/DCs
	PMNs
	Th1 cells
	Th17 cells
Tubulointerstitial nephritis	Activation of peritubular endothelial cells and tubular epithelial cells by proinflammatory cytokines
	Peritubular vascular injury by ICs
	Amplification of inflammation via release of cytokines and cytotoxic factors
	Cellular autoimmunity:
	Tertiary lymphoid organ formation and immunoglobulin production
	Anti-matrical and anti-epithelial cell autoantibodies from systemic circulation

Abbreviation: IC, immune complex.