Antibody response to recombinant 65-kDa, 70-kDa and 18-kDa mycobacterial antigens in leprosy patients and healthy contacts in a leprosy-endemic population.Int J Lepr Other Mycobact Dis. 1994 Jun; 62(2):245-55.IJ
Antibody responses to recombinant Mycobacterium leprae 65-kDa (rML65) and 18-kDa (rML18), M. bovis BCG 65-kDa (rMB65) and M. tuberculosis 70-kDa (rMT70) antigens were measured by indirect ELISA in sera from leprosy patients and healthy contacts in a leprosy-endemic area in southern India. Antibody responses to M. leprae-specific epitopes on phenolic glycolipid-I (PGL-I) and a 35-kDa protein antigens also were measured simultaneously by PGL-I ELISA and the serum antibody competition test (SACT), respectively. Significantly higher levels of antibodies of the IgG isotype to rML65 and rMB65 were observed in bacterial index (BI)-positive, lepromatous (LBI+) patients but not in other groups of leprosy patients and endemic controls [healthy family contacts (HFC), healthy hospital contacts (HHC), and healthy non-contacts (HNC)]. LBI+ patients could be distinguished from LBI- patients on the basis of their higher levels of IgG antibodies to rML65, rMB65 and rMT70; lower levels of IgM antibodies to these antigens and higher levels of anti-PGL-I IgM levels. In the former group, 84% were SACT positive in contrast to 39% in the latter groups. Among lepromatous patients good positive correlations were observed between IgG antibody responses to rML65 and rMB65 and anti-PGL-I IgM levels, SACT ID50 titers as well as BIs. Among healthy controls, HFC had higher levels of IgG antibodies to rML65, but lower levels to rMB65 than did HNC. Thirty-nine percent of the HFC were seropositive to anti-PGL-I IgM antibodies in contrast to 4% in the HNC. On the basis of these criteria, the immune profile of the HFC appears to be distinctly different from that of the HNC, even though both groups are from the same endemic area. It is therefore possible that antibody response to defined protein antigens of mycobacteria is influenced by the lesional bacterial load in leprosy patients and by exposure to homologous proteins of M. leprae and/or related environmental mycobacteria in the case of healthy contacts and noncontacts. The above results are discussed in relation to T- and B-cell activity toward M. leprae antigens and the immunoregulatory mechanisms of antibody production in leprosy.