02738nas a2200385   4500000000100000008004100001260001300042653001500055653001000070653000900080653002400089653001900113653001200132653001100144653001100155653002300166653002400189653001200213653002600225653000900251653001600260653002500276653002400301653001500325653001700340100001500357700001200372700001300384245025600397856004100653300001100694490000700705520162600712022001402338       1982                            d  c1982 Dec10aAdolescent10aAdult10aAged10aAntigens, Bacterial10aConcanavalin A10aDapsone10aFemale10aHumans10aImmunity, Cellular10aIn Vitro Techniques10aleprosy10aLymphocyte Activation10aMale10aMiddle Aged10aMycobacterium leprae10aPhytohemagglutinins10aTuberculin10aTuberculosis1 aReitan L J1 aCloss O1 aBelehu A00aIn vitro lymphocyte stimulation in patients with lepromatous and borderline tuberculoid leprosy. The effect of dapsone treatment on the response to Mycobacterium leprae antigens, tuberculin purified protein derivative and non-mycobacterial stimulants.  uhttp://ila.ilsl.br/pdfs/v50n4a05.pdf  a455-670 v503 a<p>Lymphocytes from peripheral blood were isolated from leprosy patients and healthy contacts (HC) of leprosy patients and stimulated in vitro with: Mycobacterium leprae and a M. leprae cell wall antigen, MLW 1; tuberculin purified protein derivative (PPD); antigens prepared from Candida albicans, Entamoeba histolytica, Leishmania aethiopica, and parotitis virus; the non-specific mitogens phytohemagglutinin (PHA) and concanavalin A (Con-A). Lymphocytes from patients with untreated lepromatous leprosy failed to respond to the M. leprae antigens, and the median response to PPD was also significantly (p less than 0.005) lower than in the HC group. They responded almost as well as the other groups to non-mycobacterial antigens, PHA, and Con-A. In LL patients who had been treated with dapsone for several (median 10) years, the failure to respond to M. leprae antigens remained, but the depression of the PPD response and the slight non-specific depression of the lymphocyte stimulation test (LST) responsiveness had been reversed. Our results confirm that the major defect in the cell-mediated immune response of LL patients is M. leprae-specific and permanent. The possibility that the defect may be due to a continuous, antigen-induced suppression of the immune response is discussed. That the defect also affected the response to PPD is important since it points to a clear antigenic relationship between M. leprae and BCG/M. tuberculosis. Evidence is presented suggesting that an antigen induced suppressor mechanism may be operating in vitro with cells from patients with borderline tuberculoid leprosy.</p>
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