02673nas a2200409   4500000000100000008004100001260001300042653002600055653002700081653002500108653002400133653002300157653001800180653001600198653001600214653001100230653002500241653001200266653002400278653001600302653002500318653003000343653002600373653001800399100001500417700001200432700001400444700001400458700001200472700001000484245026000494856007000754300001300824490000800837520140400845022001402249       1999                            d  c1999 Jun10aAntibodies, Bacterial10aAntibodies, Monoclonal10aAntibody Specificity10aAntigens, Bacterial10aBacterial Proteins10aChaperonin 6010aChaperonins10aGlycolipids10aHumans10aImmunohistochemistry10aleprosy10aLipopolysaccharides10aMacrophages10aMycobacterium leprae10aPredictive Value of Tests10aRetrospective Studies10aSkin Diseases1 aVerhagen C1 aFaber W1 aKlatser P1 aBuffing A1 aNaafs B1 aDas P00aImmunohistological analysis of in situ expression of mycobacterial antigens in skin lesions of leprosy patients across the histopathological spectrum. Association of Mycobacterial lipoarabinomannan (LAM) and Mycobacterium leprae phenolic glycolipid-I (PGL  uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277205/pdf/1751.pdf  a1793-8040 v1543 a<p>The presence of mycobacterial antigens in leprosy skin lesions was studied by immunohistological methods using monoclonal antibodies (MAbs) to Mycobacterium leprae-specific phenolic glycolipid I (PGL-I) and to cross-reactive mycobacterial antigens of 36 kd, 65 kd, and lipoarabinomannan (LAM). The staining patterns with MAb to 36 kd and 65 kd were heterogeneous and were also seen in the lesions of other skin diseases. The in situ staining of PGL-I and LAM was seen only in leprosy. Both antigens were abundantly present in infiltrating macrophages in the lesions of untreated multibacillary (MB) patients, whereas only PGL-I was occasionally seen in scattered macrophages in untreated paucibacillary lesions. During treatment, clearance of PGL-I from granulomas in MB lesions occurred before that of LAM, although the former persisted in scattered macrophages in some treated patients. This persistence of PGL-I in the lesions paralleled high serum anti-PGL-I antibody titers but was not indicative for the presence of viable bacilli in the lesions. Interestingly, we also observed a differential expression pattern of PGL-I and LAM in the lesions of MB patients with reactions during the course of the disease as compared with those without reactions. In conclusion, the in situ expression pattern of PGL-I and LAM in MB patients may assist in early diagnosis of reactions versus relapse.</p>  a0002-9440