Review ArticleUnraveling the immunopathogenesis of glomerular disease

- Immune-mediated damage to the glomerulus drives the pathogenesis of glomerular diseases.
- Both innate and adaptive immune cells and their mediators contribute to glomerular damage.
- Nephritic syndrome is characterized by the infiltration of inflammatory cells into the mesangium and subendothelium.
- Nephrotic syndrome is characterized by damage to podocytes driven by immune complexes in the subepithelial space.
- Design of new therapies to treat glomerular disease requires further elucidation of the immune mechanisms involved.

Immune-mediated damage to glomerular structures is largely responsible for the pathology associated with the majority of glomerular diseases. Therefore, a detailed understanding of the basic immune mechanisms responsible for glomerular damage is needed to inform the design of novel intervention strategies. Glomerular injury of immune origin is complex and involves both inflammatory and non-inflammatory processes driven by elements of the innate and adaptive immune system. This review summarizes the basic immune mechanisms that cause glomerular injury leading to the nephritic and nephrotic syndromes. A major focus of the review is to highlight the mechanisms by which antibodies cause glomerular injury through their interactions with glomerular cells, complement proteins, phagocytes bearing complement and Fcγ receptors, and dendritic cells expressing the neonatal receptor for IgG, FcRn.