02045nas a2200373   4500000000100000008004100001260001300042653001500055653001000070653002400080653001800104653001300122653001100135653001100146653001200157653002600169653000900195653001600204653003100220653001500251653001800266100001300284700001400297700001400311700002000325700001300345245010800358856005900466300001000525490000700535050003200542520108300574022001401657       1995                            d  c1995 Mar10aAdolescent10aAdult10aAntigens, Bacterial10aClonal Anergy10aEpitopes10aFemale10aHumans10aleprosy10aLymphocyte Activation10aMale10aMiddle Aged10aMycobacterium tuberculosis10aSkin Tests10aT-Lymphocytes1 aKaleab B1 aWondimu A1 aLikassa R1 aWoldehawariat N1 aIvanyi J00aSustained T-cell reactivity to Mycobacterium tuberculosis specific antigens in 'split-anergic' leprosy.  uhttp://leprev.ilsl.br/pdfs/1995/v66n1/pdf/v66n1a03.pdf  a19-250 v66  aInfolep Library - available3 a<p>Split anergy represented by delayed-type hypersensitivity skin reaction to tuberculin, but not to leprosin, is known to occur in a distinct proportion of leprosy patients. The mechanism was originally attributed to Mycobacterium leprae-specific suppression of T cells toward common mycobacterial antigens. This study ascertained an alternative explanation, attributing the phenomenon to selective responsiveness to M. tuberculosis-specific epitopes. Indeed, the results of blood T-cell proliferative responses in 11 split-anergic patients showed normal responsiveness to the M. tuberculosis-specific 38 kDa lipoprotein and peptide 71-91 of the 16 kDa antigen but diminished responsiveness to 2 common mycobacterial antigens, represented by the 65 kDa heat shock protein and the fibronectin-binding Ag85 complex, as compared with leprosin responsive patients and healthy contacts. These findings support the hypothesis that split anergy is due to selective recognition of M. tuberculosis-specific epitopes and deletion of T cells reacting to shared mycobacterial antigens.</p>  a0305-7518