T helper (Th) cells belong to the adaptive immune system and provide an effective and
antigen-specific means of host protection. Th17 cells are a subset of Th cells, characterized by the production of the inflammatory
cytokines interleukin (IL)-17A (IL-17A) and
IL-17F, which bind to a receptor complex comprised of IL-17RA and IL-17RC subunits. Th17 cells combat extracellular and
fungal infections, but have been implicated in
autoimmune diseases. In many autoimmune conditions, the dysregulated immune response involves several parts of the immune system, including
autoantibodies, B and T cells. Targeted
biological therapies are appealing, as they may prevent unwanted side effects in patients. There is evolving evidence that Th17 cells are important in the kidney, mediating injury in response to vascular or chemical insults to the renal tubules, and in
autoimmune diseases of the glomerulus, either through a specific attack on the glomerular basement membrane or as part of a generalized systemic inflammatory disease.
Therapies targeting
IL-17A,
IL-12p40 and IL-17RA are being explored in clinical trials or are being utilized in clinical practice for the treatment of other
IL-17 mediated diseases, such as
psoriasis. This review explores the current evidence that
IL-17A and Th17 cells may be pathogenic in immune
kidney disease, including
anti-glomerular basement membrane disease,
antineutrophil cytoplasmic antibody associated
vasculitis and
lupus nephritis, as well as in
acute kidney injury. It will discuss the place that
biological agents against
IL-17A,
IL-12p40 and IL-17RA may have in the treatment of these conditions.