Search PubMed⌕ Search

PubMed · 2449998

Mast cell polymorphisms. Present concepts, future directions.

Abstract

Although mast cells are widely distributed in the body, their functions are poorly known. The elucidation of mast cell function is complicated by growing evidence that mast cells are heterogeneous. Recent studies of mast cell ontogeny suggest that microenvironmental stimuli control the phenotypic expression of parts of the genome leading to subtype differences in a common lineage. Mast cells influence cell proliferation, differentiation, and activation in a range of target cells, although until recently they were considered important only in immediate hypersensitivity. However, they function in delayed-type hypersensitivity, potentiate cytotoxicity of eosinophils and macrophages, and are cytotoxic for certain targets themselves. Mast cell mediators influence blood flow and vascular permeability and facilitate angiogenesis. Numerous mast cell mediators are immunoregulatory. In vitro experiments have begun to investigate the role of mast cells in fibrotic diseases. Further knowledge of mast cell heterogeneity will provide the basis for new therapies in inflammatory diseases of the intestine and other organs.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D Befus, H Fujimaki, T D Lee, M Swieter. 1988. Mast cell polymorphisms. Present concepts, future directions.. https://doi.org/10.1007/bf01538127

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Hypothesis about mechanisms through which nicotine might exert its effect on the interdependence of inflammation and gut barrier function in ulcerative colitis.

Ulcerative colitis (UC) is characterized by impairment of the epithelial barrier and the formation of ulcer-type lesions, which result in local leaks and generalized alterations of mucosal tight junctions. Ultimately, this results in increased basal permeability. Although disruption of the epithelial barrier in the gut is a hallmark of inflammatory bowel disease and intestinal infections, it remains unclear whether barrier breakdown is an initiating event of UC or rather a consequence of an underlying inflammation, evidenced by increased production of proinflammatory cytokines. UC is less common in smokers, suggesting that the nicotine in cigarettes may ameliorate disease severity. The mechanism behind this therapeutic effect is still not fully understood, and indeed it remains unclear if nicotine is the true protective agent in cigarettes. Nicotine is metabolized in the body into a variety of metabolites and can also be degraded to form various breakdown products. It is possible these metabolites or degradation products may be the true protective or curative agents. A greater understanding of the pharmacodynamics and kinetics of nicotine in relation to the immune system and enhanced knowledge of gut permeability defects in UC are required to establish the exact protective nature of nicotine and its metabolites in UC. This review suggests possible hypotheses for the protective mechanism of nicotine in UC, highlighting the relationship between gut permeability and inflammation, and indicates where in the pathogenesis of the disease nicotine may mediate its effect.

Colitis, Ulcerative↗