Genetically modified immune responses to infections and self-antigens initiate most forms of
GN by generating pathogen-and danger-associated molecular patterns that stimulate Toll-
like receptors and complement. These innate immune responses activate circulating
monocytes and resident glomerular cells to release inflammatory mediators and initiate
adaptive, antigen-specific immune responses that collectively damage glomerular
structures. CD4 T cells are needed for B cell–driven antibody production that leads to …