02076nas a2200313   4500000000100000008004100001260001300042653001400055653002100069653001100090653002200101653002500123653003700148653001800185653003200203100001500235700001400250700001600264700001200280700001200292700001500304700001200319700001200331245008000343300001100423490000700434520130700441022001401748       2005                            d  c2005 Oct10aApoptosis10aCell Line, Tumor10aHumans10aLymphotoxin-alpha10aMycobacterium leprae10aReceptors, Tumor Necrosis Factor10aSchwann Cells10aTumor Necrosis Factor-alpha1 aOliveira R1 aSampaio E1 aAarestrup F1 aTeles R1 aSilva T1 aOliveira A1 aAntas P1 aSarno E00aCytokines and Mycobacterium leprae induce apoptosis in human Schwann cells.  a882-900 v643 a<p>The development of deformities during the course of leprosy disease is a major public health concern worldwide. It is possible that cytokine production and apoptosis of Schwann cells (SCs) directly affect nerve degeneration and regeneration leading to injury of the myelin sheath and axon. In the present study, the expression of TNFalpha, TGFbeta, and their receptors, in addition to cell death triggered by cytokines or whole Mycobacterium leprae were investigated in a human SC line. The results showed the presence of TNF-Rs and TGF-RII on the SC membrane and the shedding of TNF-Rs during the culture period. Evaluation of cell death was performed through TUNEL and flow cytometry techniques. TNFalpha/TGFbeta combination as well as M. leprae infection triggered an increase in the apoptosis rate in the cultured SC. Moreover, reverse transcriptase-polymerase chain reaction assay revealed that M. leprae upregulated the expression of such cytokines and their receptors on the SC line. Despite the detection of TNFalpha mRNA, no protein was found in the culture supernatants. The data indicate that induction of SC death after cell interaction with M. leprae may, in fact, be implicated in the pathogenesis of nerve damage, which can most likely be modulated by in vivo cytokine production.</p>  a0022-3069