Our data suggest that in leprosy, RAGE and EN-RAGE may be involved in the proinflammatory process rather than the antimycobacterial activity, especially during the lepra reaction. The blockade of the interaction of RAGE and EN-RAGE at the early stage of the inflammatory process may minimize the inflammatory response and consequent tissue damage or the sequelae of leprosy.

SUMMARYAnti-neural antibodies have been implicated to play a role in the pathogenesis of nerve damage in leprosy patients. To find the relationship between anti-neural antibodies and clinical findings, we attempted to detect antibodies against iieurofilament-enriched proteins by ELISA in ,sera from leprosy patients. Of 2S9 sera frotn leprosy patients, 74 (256''..) had signilicant anti-neural antibodies; ineontrasl. 1 (50".,.) of 20 tuberculosis patients and II (71%) of 154 controls were seroreactive lo nerve antigen. When clinical types were considered, a significant level of anti-ncural IgG antibodies was detectable in 53(30 !"•;,) of 176 sera from lepromatous patients compared with 21 (18 6";0of 113 ,'«:ra from tuberculoid palients, indicating that lepromatous palients were more likely to be seropositive to nerve antigens in ELISA. Some of the ELlSA-reactive sera showed antibody reactivity with 38-kD. 40-kD and 43-kD nerve antigens in Western blotting analysis. There was no apparent correlation between seroreactivity to nerve antigens and bacterial load in leprosy patients. Although there was no statistical significance, anti-neural antibodies were detectable more often aiuonij; ilic patients on chemotherapy ihan the untreated and among the patients with erythema nodosum leprosum than without. The results, therefore, suggest that anti-neural antibodies are elicited during the course of leprosy and may be associated with the extensiveness of nerve involvement in the patienis.