Leprosy, a chronic granulomatous infection of man caused by Mycobacterium leprae, is essentially a disease affecting the nervous system. However, the mechanisms implicated in nerve damages in leprosy patients are still not well understood. The
similarties of pathological features, such as demyelination and/or axonal destruction, observed in Guillian-Barre syndrome (GBS) and IgM polyneuropathy as well as in leprous polyneuropathy strongly suggest an involvement of autoimmune response
leading
to the nerve damage in leprosy as in GBS or IgM polyneuropathy. To elucidate such possibility, this study was undertaken to detect anti-neural antibodies in the sera of leprosy patients and to characterize further the antigens reacting with these
antibodies.
@ES The results obtained were as follows.
@EN 1. The anti-neural antibodies were detected by enzyme linked immunosorbent assay (ELISA) in 74(25.6%) of the 289 leprosy patients and in 11(7.1%) of the 154 healthy subjects and the difference between these two groups was highly
significant(p<0.005). Among leprosy patients it was significantly higher in the lepromatous type than in the tuberculoid (p<0.05).
2. The anti-neural antibodies detected did not cross-react with human peripheral blood monocytes or RBCs, but seemed to react with some of mycobacterial antigens.
3. In Western blotting, anti-neural antibodies reacted mainly with three antigens having molecular weights of 38kD, 40kD and 43kD, respectively.
4. The immunohistological study using immunofluorescence assay showed that the antigens reacting with anti-neural antibodies were distributed diffusely in the cervical spinal section, especially in the gray matter. Some cells showed an intense
fluorescence around its membranes.
5. There was no relationship between the bacterial indices of lepromatous leprosy patients and their anti-neural antibodies.
6. The anti-neural antibodies were slightly but not significantly increased in patients with the complication of erythema nodosum leprosum as compare to those without complication.
7. The prevalence of anti-neural antibodies was higher in the patients who had the disease history for more than 5 years those for less than 5 years(p<0.05).
In conclusion, since specific antibodies against human nervous tissue are increased in leprosy patients, it is suggested that the autoimmune response to the nervous tissues may play a role in nerve damage in leprosy.
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