Innate immunity and IgA nephropathy.
The hallmark of IgA nephropathy (IgAN) is macroscopic hematuria coinciding with, or immediately following, a mucosal infection, usually of the upper respiratory airways. The role of mucosal pathogens has been proven in different experimental models. Mucosal (or innate) immunity acts through the recognition of pathogen-associated molecular patterns by macrophages, dendritic cells, leukocytes and other cells, and favors opsonization and phagocytosis. Then, mature dendritic cells interact with lymphocytes leading to activation of specific T cell and antibody synthesis. A dysregulation of innate immunity in IgAN is likely to result in failure of mucosal antigen elimination and/or altered IgA synthesis as well as inflammation. Complement system activation is a relevant arm of the innate immunity armamentarium and is associated with IgAN activity and progression. Other powerful mediators of mucosal immunity, Toll-like receptors (TLRs), were reported to modulate the severity of IgAN in ddy mice spontaneously developing IgA deposits, while some new data in peripheral lymphomonocytes of patients with IgAN show TLR hyperexpression particularly during phases of clinical activity. The involvement of innate immunity in IgAN represents a new, exciting field of research.
Coppo
Rosanna
R
Nephrology, Dialysis and Transplantation, Regina Margherita Children's University Hospital, Piazza Polonia 94, Turin, Italy. rosanna.coppo@unito.it
Amore
Alessandro
A
Peruzzi
Licia
L
Vergano
Luca
L
Camilla
Roberta
R
D000818:Animals; D003167:Complement Activation; D005922:Glomerulonephritis, IGA / Q000209:etiology / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D018928:Immunity, Mucosal; D051379:Mice; D051193:Toll-Like Receptors / Q000502:physiology
D051193:Toll-Like Receptors