02822nas a2200373 4500000000100000008004100001260001300042653002400055653004400079653001300123653001100136653001800147653001200165653002600177653002500203653003100228653001800259653001400277100001400291700001100305700001300316700001300329700001600342700001400358700001500372700001300387700001500400245017100415856009000586300000900676490000700685520174200692022001402434 1986 d c1986 Apr10aAntigens, Bacterial10aDose-Response Relationship, Immunologic10aEpitopes10aHumans10aInterleukin-210aleprosy10aLymphocyte Activation10aMycobacterium leprae10aMycobacterium tuberculosis10aT-Lymphocytes10aThymidine1 aBarnass S1 aMace J1 aSteele J1 aTorres P1 aGervasoni B1 aRavioli R1 aTERENCIO J1 aRook G A1 aWaters M F00aPrevalence and specificity of the enhancing effect of three types of interleukin 2 on T cell responsiveness in 97 lepromatous leprosy patients of mixed ethnic origin. uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1542157/pdf/clinexpimmunol00121-0050.pdf a41-90 v643 a

Peripheral blood mononuclear cells from 97 predominantly lepromatous leprosy patients and 11 control subjects were tested in a lymphoproliferative assay for response to Mycobacterium leprae (whole and sonicated), and sonicated M. vaccae, M. tuberculosis, and M. scrofulaceum, in the presence and absence of three types of interleukin 2 (IL-2) (crude, purified, and recombinant). IL-2 enhanced the response to sonicated M. tuberculosis and M. leprae organisms more often in patients than in control subjects, but not significantly so and only in a minority of patients. This effect was significantly more common (though still only found in a minority of 46%) using M. leprae organisms as antigen, than when using sonicates of M. leprae (19%) or M. vaccae (19%). However it was nearly as frequent using sonicated M. tuberculosis, or M. scrofulaceum. Thus in only nine patients was the effect specific to M. leprae. Enhancement by IL-2 could not be related to the type of IL-2 used, the dose of antigen, or the amount of endogenous IL-2 released by the cells tested. Similarly it was not related to the extent to which IL-2 caused increased background proliferation in control wells, which occurred to an equal extent using cells from control subjects, nor was it related to the extent of antigen-driven proliferation. The data have also been analysed in relation to duration of disease (50 years to a few weeks) and ethnic origin. No correlations have been revealed. Thus enhancement by IL-2 of the lymphoproliferative response to mycobacterial antigens does occur using cells from lepromatous leprosy patients, but it is found in a minority of patients, it is not specific to M. leprae, and can occur with cells from normal donors.

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