Experimental allergic arthritis in mice: Factors determining chronicity and tissue destruction
Chronicity of inflammation can be understood in terms of the continuous presence of an inflammatory stimulus. This may be generated by an abundant supply from the circulation, e.g. through the daily antigenic and bacterial load at the gastrointestinal tract, local retention at special sites, or induction of autoimmune phenomena. Evidence for the importance of local antigen retention in chronicity of joint inflammation has emerged from studies in the antigen induced arthritis model in the rabbit. We have recently found that the principle of local antigen retention is also important for chronicity in the mouse model. Using this latter model evidence was obtained that antigen from the circulation, present either after intravenous or oral administration, may play a role in exacerbations (flare-up) of chronic smouldering arthritis. The present paper summarizes our findings in the antigen induced arthritis model in the mouse, including tissue destruction, factors determining local retention of proteins (antigens) in the joint, and the conditions needed for the occurrence of the flare-up phenomenon.
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