Free radicals, immunoglobulins and complement as mediators of inflammation.
There is evidence for both oxygen-centred free radicals and products of complement activation acting as mediators of inflammation. Evidence for the generation and reaction of free radicals at sites of inflammation can only be indirect and circumstantial due to their very transient nature. Evidence for complement activation in several inflammatory conditions, including rheumatoid arthritis is strong. These mediator classes individually possess a range of potential proinflammatory activities. Their effects may be linked through the formation of immune complexes and the activation of polymorphonuclear leukocytes. Their actions will also be linked with and modulated by the activities of other mediators mentioned only briefly in this chapter. The relative importance of the different mediators in any particular inflammatory condition is difficult to ascertain. The importance of free radicals and complement will be better understood when drugs specifically and unequivocally aimed at their control are identified. This potential for therapeutic advances in the treatment of inflammatory disorders has yet to be realized.
Roberts
N A
NA
D000818:Animals; D000936:Antigen-Antibody Complex / Q000502:physiology; D001168:Arthritis / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000378:metabolism; D003165:Complement System Proteins / Q000502:physiology*; D005609:Free Radicals; D006801:Humans; D006878:Hydroxides / Q000502:physiology*; D007136:Immunoglobulins / Q000502:physiology*; D013481:Superoxides / Q000502:physiology*
D000936:Antigen-Antibody Complex; D005609:Free Radicals; D006878:Hydroxides; D007136:Immunoglobulins; D013481:Superoxides; D003165:Complement System Proteins