Effects of biomaterial-induced inflammation on fibrosis and rejection.
Evidence is emerging that biomaterials cause inflammation by ligating innate immune receptors on antigen presenting cells. Although inflammation is usually viewed as detrimental, it has unexpected and potentially beneficial effects on fibrosis and transplant rejection. For example, the magnitude of inflammation due to a biomaterial is not predictive of the extent of fibrosis. Similarly, biomaterials do not always show adjuvancy. Some biomaterials suppressed T cell rejection responses in vivo and in vitro, while others non-specifically stimulated T cell proliferation. Understanding these complex inter-relationships is the key to designing a biomaterial that stimulates regeneration and induces tolerance in tissue engineering applications.
Jones
Kim S
KS
Department of Chemical Engineering, McMaster University, Hamilton, Ontario, L8S 4L7 Canada. kjones@mcmaster.ca
D000276:Adjuvants, Immunologic / Q000009:adverse effects; D000818:Animals; D001672:Biocompatible Materials / Q000009:adverse effects*; D002465:Cell Movement; D006224:Cricetinae; D005355:Fibrosis; D006084:Graft Rejection / Q000209:etiology / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000276:immunology; D008262:Macrophage Activation; D051379:Mice; D051192:Receptors, Pattern Recognition / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D023822:Tissue Engineering; D023001:Transplantation Tolerance
D000276:Adjuvants, Immunologic; D001672:Biocompatible Materials; D051192:Receptors, Pattern Recognition