Published 2015:

Silicosis is suspected to be an immune disease, involving activation of primitive highly conserved genes, like those involved in the Toll-Like Receptor (TLR) pathway. Following these hypothesis, progression from silica dust deposition in lung parenchyma to diffuse fibrosis, silicotic nodule formation and, finally, honeycombing, would be accelerated in presence of favourable genetic pattern, explaining the presence of rapidly progressive pattern also for low environmental or occupational silica dust exposure.

IgA nephropathy, the most common type of glomerulonephritis worldwide, is also suspected as an immune disease. Genetic or acquired abnormalities of immune system would be a trigger for increased production of IgA, which deposition in glomerulus induces and propagates renal disorder.