Figure 1.

Schema of progression of SLE to end organ renal disease (LN). After the onset of SLE in a genetically susceptible individual, there is involvement of multiple cells types involving both innate and adaptive immune systems. The antigen presenting cells (APC) present self-antigens from various sources to T lymphocytes, which results in generation of auto reactive T cells with low activation threshold. These CD4 T lymphocytes in turn instruct B cells to produce autoantibodies (Y) of different specificities. Not much is known about the cause and initiation of renal disease, but in-situ generated or circulating immune complex (IC) deposits in the glomeruli are the most plausible culprits. This leads to progressive glomerular pathology and secretion of chemokines, cytokines and matrix proteins, resulting in immune cell infiltration and tissue damage. Loss of glomerular permeability also leads to tubulointerstitial injury which is perpetuated by intrinsic tubular cell inflammatory phenotype and infiltrating immune cells which eventually leads to renal failure.