Collagen deposition in autoimmune diseases: the expanding role of the fibroblast in human fibrotic disease.
Fibrosis, usually considered an extension of the normal process of wound healing, follows to a variable degree host responses of an inflammatory nature, both immune and non-immune. The immediate mesenchymal effector cell of fibrosis, the fibroblast, has more or less been taken for granted in this process, due largely to its monotonous morphological uniformity. An emerging realization that the fibroblast can react in a variety of ways, both as an amplifying population of cells and in selective ways as the final arbiter of the extracellular matrix, is the subject of this report. This heterogeneity of fibroblast behaviour is characterized and, since many types of cells (endothelial, smooth muscle, epithelial) have now been shown to respond to matrix-derived signals, the potential for mesenchymal cell selection as a mechanism for understanding human fibrotic disease is probed. Signals which selectively alter fibroblast proliferation and fibroblast phenotypic expression are emphasized.
D000375:Aging; D001327:Autoimmune Diseases / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism*; D003240:Connective Tissue Diseases / Q000276:immunology* / Q000378:metabolism; D005347:Fibroblasts / Q000502:physiology*; D006801:Humans; D012879:Skin Physiological Phenomena
D003094:Collagen