Toll-like receptors: emerging concepts in kidney disease

Curr Opin Nephrol Hypertens. 2007 May;16(3):177-83. doi: 10.1097/MNH.0b013e32803fb767.

Abstract

Purpose of review: To summarize the recent advances in the role of Toll-like receptors (TLRs) in innate immunity, with a special focus on recent studies addressing the expression and function of TLRs in kidney disease.

Recent findings: Pathogen-recognition receptors including TLRs mediate immune activation upon pathogen recognition in different extracellular and intracellular compartments. In contrast to professional antigen-presenting cells, renal cells express a limited pattern of TLR (i.e. express TLR1-TLR6 but lack expression of the endosomal TLR7-TLR9). TLRs on renal cells contribute to the innate immune response in renal infection. Furthermore, recent studies provide experimental evidence for the functional role of TLRs in immune complex disease and autoimmunity. Furthermore, the recognition of endogenous molecules released from injured cells such as biglycan or heat-shock proteins may contribute to acute tubular injury and seem to provide adjuvant activity for renal inflammation. Furthermore, TLR7 and TLR9 are involved in the pathogenesis of lupus nephritis.

Summary: The field of TLR research elucidates the molecular mechanisms of infection-associated kidney diseases but may also further support the concept that innate immunity significantly contributes to the so-called types of nonimmune kidney diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bacterial Infections / complications*
  • Bacterial Infections / immunology
  • Dendritic Cells / immunology
  • Glomerulonephritis / etiology
  • Glomerulonephritis / immunology
  • Humans
  • Immunity, Innate*
  • Kidney / immunology*
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Diseases / etiology
  • Kidney Diseases / immunology
  • Ligands
  • Lupus Nephritis / etiology
  • Lupus Nephritis / immunology
  • Macrophages / immunology
  • Nephritis / etiology
  • Nephritis / immunology*
  • Nephritis / metabolism
  • Nephritis / physiopathology
  • Toll-Like Receptors / immunology*
  • Toll-Like Receptors / metabolism
  • Virus Diseases / complications*
  • Virus Diseases / immunology

Substances

  • Ligands
  • Toll-Like Receptors