Mediators of immune glomerular injury

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Mediators of immune glomerular injury may be divided into primary ana secondary. Primary mediators include antibody and T cells and secondary include complement, infiltrating inflammatory cells, such as neutrophils, monocytes/macrophages and platelets, coagulation system, resident glomerular cells including mesangial, endothelial and epithelial cells, reactive oxygen metabolites, eicosanoids, proteolytic enzymes and a host of cytokines. Following initiation of immune glomerular injury with primary mediators, which in most cases is antibody, a complex set of interactions involving some or all of the secondary mediators occurs in the glomerulus, ultimately leading to the clinical manifestations of glomerular injury. The precise sequence and the mechanisms of these interactions are not fully defined but are under intense study. The identity of the putative antigens and why and how an autoimmune response develops are also not fully known.

Original languageEnglish (US)
Pages (from-to)324-336
Number of pages13
JournalAmerican Journal of Nephrology
Volume13
Issue number5
StatePublished - 1993

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Wounds and Injuries
Mesangial Cells
Eicosanoids
Antibodies
Autoimmunity
Monocytes
Neutrophils
Peptide Hydrolases
Blood Platelets
Endothelial Cells
Epithelial Cells
Macrophages
Cytokines
Oxygen
T-Lymphocytes
Antigens

Keywords

  • Antibody
  • Autoantibody
  • Complement
  • Cytokines
  • Eicosanoids
  • Glomerular cells
  • Glomerular injury
  • Glomerulonephritis
  • Heymann nephritis
  • Immune injury

ASJC Scopus subject areas

  • Nephrology

Cite this

Mediators of immune glomerular injury. / Makker, Sudesh P.

In: American Journal of Nephrology, Vol. 13, No. 5, 1993, p. 324-336.

Research output: Contribution to journalArticle

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