Mast cells find their way to the kidney

Abstract

Histologically, progressive renal disease is characterized by an interstitial infiltrate of inflammatory cells in association with tubular atrophy and interstitial fibrosis. There are many reasons to believe that the mononuclear cells, especially those of monocytic lineage, play an active role in fibrogenesis even though definitive proof of their role is still lacking1. In this issue of Kidney International, El-Koraie et al investigate the presence of mast cells in the interstitium of human kidney biopsies obtained from patients with chronic glomerulonephritis2. Mast cells turn out to be a very interesting population of bone marrow–derived cells that have been largely ignored by the nephrology community. These basophilic leukocytes are characterized by the presence of cytoplasmic granules enriched with proteoglycans and proteases, including the mast cell–specific proteases, chymase and tryptase. Mast cell precursor cells originate in the bone marrow, circulate in small numbers in the blood, and mature into tissue mast cells within most organs. Mast cells are best known for their role in anaphylactic allergic reactions following interactions of immunoglobulin E (IgE) with the Fc epsilon receptor 1. Mature tissue mast cells are heterogenous, with at least two phenotypically distinct populations identified. In rodents, T-cell–dependent mucosal-type mast cells can be distinguished from T-cell–independent connective tissue–type mast cells by their differential staining with alcian blue-safarin and by differences in the content of their granules (histamine, proteoglycans, and serine proteases). In humans, it is not currently possible to distinguish between mucosal-type and connective tissue–type mast cells. Human mast cells are subtyped on the basis of mast cell–specific proteases. All human mast cells contain tryptase, the major mast cell protein constituent, whereas only a subset contains chymase.