Mast cells and inflammatory kidney disease

Ulrich Blank, Marie Essig, Lisa Scandiuzzi, Marc Benhamou, Yutaka Kanamaru

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Inflammatory kidney disease involves a complex network of interactions between resident kidney and infiltrating hematopoietic cells. Mast cells (MCs) are constitutively found in kidneys in small numbers but increase considerably in various renal diseases. While this increase is usually interpreted as a sign of pathological involvement, recent data using MC-deficient animals show their ability to restore kidney homeostasis. In anti-glomerular basement membrane antibody-induced glomerulonephritis, MCs are protective by initiating repair and remodeling functions counteracting the devastating effects of glomerular injury. Protection may also include immunoregulatory capacities to limit autoreactive T-cell responses. MCs also control tubulointerstitial fibrosis by activating tissue remodeling and neutralizing fibrotic factors. Release of mediators by MCs during inflammation, however, could also promote unwanted responses that ultimately lead to destruction of kidney structure, as exemplified by data showing either protection or aggravation in related renal disease models. Similarly, while the action of proteases may initially be beneficial, the generation of fibrosis-promoting angiotensin II by chymase also shows the limits of adaptive responses to achieve homeostasis. Thus, it is likely the physiological context involving the interaction with other cells and inflammatory mediators that determines the final action of MCs in the development of kidney disease.

Original languageEnglish (US)
Pages (from-to)79-95
Number of pages17
JournalImmunological Reviews
Volume217
Issue number1
DOIs
StatePublished - Jun 2007
Externally publishedYes

Fingerprint

Kidney Diseases
Mast Cells
Kidney
Homeostasis
Fibrosis
Chymases
Glomerular Basement Membrane
Glomerulonephritis
Angiotensin II
Peptide Hydrolases
Inflammation
T-Lymphocytes
Antibodies
Wounds and Injuries

Keywords

  • End-stage renal failure
  • Fibrosis
  • Glomerulonephritis
  • Inflammation
  • Kidney disease
  • Mast cell

ASJC Scopus subject areas

  • Immunology

Cite this

Blank, U., Essig, M., Scandiuzzi, L., Benhamou, M., & Kanamaru, Y. (2007). Mast cells and inflammatory kidney disease. Immunological Reviews, 217(1), 79-95. https://doi.org/10.1111/j.1600-065X.2007.00503.x

Mast cells and inflammatory kidney disease. / Blank, Ulrich; Essig, Marie; Scandiuzzi, Lisa; Benhamou, Marc; Kanamaru, Yutaka.

In: Immunological Reviews, Vol. 217, No. 1, 06.2007, p. 79-95.

Research output: Contribution to journalArticle

Blank, U, Essig, M, Scandiuzzi, L, Benhamou, M & Kanamaru, Y 2007, 'Mast cells and inflammatory kidney disease', Immunological Reviews, vol. 217, no. 1, pp. 79-95. https://doi.org/10.1111/j.1600-065X.2007.00503.x
Blank U, Essig M, Scandiuzzi L, Benhamou M, Kanamaru Y. Mast cells and inflammatory kidney disease. Immunological Reviews. 2007 Jun;217(1):79-95. https://doi.org/10.1111/j.1600-065X.2007.00503.x
Blank, Ulrich ; Essig, Marie ; Scandiuzzi, Lisa ; Benhamou, Marc ; Kanamaru, Yutaka. / Mast cells and inflammatory kidney disease. In: Immunological Reviews. 2007 ; Vol. 217, No. 1. pp. 79-95.
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