Host immune factors regulating fibrosis.

Mononuclear cells produce lymphokines and monokines, the function of which is to initiate the mobilization, proliferation and differentiation of additional mononuclear cells in an inflammatory site. In addition, these inflammatory cells produce biologically active mediators which modulate the functions of certain non-inflammatory cell targets. Lymphokines and monokines can stimulate chemotaxis, division, and matrix synthesis by connective tissue fibroblasts. Additional mononuclear cell-derived mediators can inhibit or suppress these fibroblast functions, implicating the host immune system in the regulation of connective tissue metabolism associated with an inflammatory response. Altering the balance of the production and/or release of these connective tissue-active agents could result in excess fibroblast growth and matrix synthesis (fibrosis) and its pathological manifestations.