Perpetuation of inflammation in uveitis.
A large number of different and predominantly non-specific mechanisms has evolved to amplify and to perpetuate inflammatory reactions. Which of these mechanisms enters into play depends upon the nature of the primary insult. Thus, pyogenic bacteria call forth polymorphonuclear leucocytes, which release enzymes and other pharmacologically active substances to enhance the response. Other organisms elicit a predominantly monocytic response, whose active monokines contribute further to the infiltration and activation of inflammatory cells. Those stimuli involving antigens act primarily upon lymphocytes, whose lymphokines contribute significantly to the amplification and perpetuation of inflammation. This paper will present examples of these and other mechanisms that enhance and prolong the inflammatory response, with special emphasis on those that contribute to immunopathological disease.
D000818:Animals; D000917:Antibody Formation; D000941:Antigens / Q000276:immunology; D007156:Immunologic Memory; D008222:Lymphokines / Q000276:immunology; D051379:Mice; D014605:Uveitis / Q000276:immunology*
D000941:Antigens; D008222:Lymphokines