01996nas a2200265 4500000000100000008004100001260001300042653002500055653002600080653003800106653001100144653002100155653001200176653002500188100002200213700001200235700001400247700001500261245009200276856009000368300001000458490000700468520124100475022001401716 1992 d c1992 May10aAnalysis of Variance10aAntibodies, Bacterial10aEnzyme-Linked Immunosorbent Assay10aHumans10aImmunoglobulin G10aleprosy10aMycobacterium leprae1 aDhandayuthapani S1 aIzumi S1 aAnandan D1 aBhatia V N00aSpecificity of IgG subclass antibodies in different clinical manifestations of leprosy. uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1554298/pdf/clinexpimmunol00049-0069.pdf a253-70 v883 a
We analysed specific IgG subclasses levels to Mycobacterium leprae sonicate extract (MSE), lipoarabinomannan B (LAM) and phenolic glycolipid I (PGL-I) in the sera of leprosy patients with different clinical manifestations. IgG2 was found to be the predominant antibody to MSE regardless of clinical manifestations, and IgG1 response was mostly seen in lepromatous patients. IgG3 reacted only rarely but IgG4 reacted relatively more in certain clinical groups such as borderline lepromatous and lepromatous with erythema nodosum leprosum (ENL) reaction. Most of the IgG subclass responses to MSE could be accounted for reactivity with LAM, suggesting that LAM is the major immunogen involved in the pathogenesis of leprosy. In contrast to LAM, PGL-I antigen showed considerably lower reactivities for IgG subclasses. An association between IgG subclass responses and clinical manifestations of leprosy was also seen. Whereas borderline lepromatous patients were found to have significantly higher levels of IgG2 and IgG4 to MSE, lepromatous patients had elevated levels of IgG1 and lower levels of IgG2. An interesting observation, however, was the significantly higher levels of IgG2 to LAM in the pure neuritic leprosy patients.
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