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We observed that allogeneic stem cell transplantation (ASCT) patients who were randomized to receive NAC 100\u2009mg\/kg\/day (<jats:italic>n<\/jats:italic>=73) had an increased prevalence of grade II\u2010V acute graft\u2010versus\u2010host disease (GvHD) compared to patients who did not receive NAC (<jats:italic>n<\/jats:italic>=87), indicating that NAC has an immunostimulatory effect in vivo. When studying the effect of NAC on T\u2010cell\u2010mediated immunity in vitro, we found that moderate levels of NAC (0.4\u20133.2\u2009mM) increased alloantigen\u2010induced proliferation, expression of activation markers CD25 and CD71 on T cells, and production of IFN\u2010\u03b3 and IL\u201010. In contrast, high concentrations of NAC (12.5\u201350\u2009mM) were suppressive, which may explain previously conflicting data. NAC did not cause an increase in expression of CD86, CD80, and CD83 on mature DCs at any concentration, whereas high concentrations suppressed DC maturation. Furthermore, T cells exposed to suppressive concentrations of NAC in a primary stimulation were highly responsive when re\u2010stimulated in the absence of NAC. To conclude, NAC appears to increase acute GvHD and has an immunostimulatory effect on alloantigen\u2010specific T cells.<\/jats:p>","DOI":"10.1002\/eji.201040589","type":"journal-article","created":{"date-parts":[[2011,1,24]],"date-time":"2011-01-24T13:41:21Z","timestamp":1295876481000},"page":"1143-1153","source":"Crossref","is-referenced-by-count":13,"title":["<i>N<\/i>\u2010acetyl\u2010<scp>L<\/scp>\u2010cysteine increases acute graft\u2010versus\u2010host disease and promotes T\u2010cell\u2010mediated immunity in vitro"],"prefix":"10.1002","volume":"41","author":[{"given":"Helen","family":"Karlsson","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Silvia","family":"Nava","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mats","family":"Remberger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zuzana","family":"Hassan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Moustapha","family":"Hassan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Olle","family":"Ringd\u00e9n","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2011,2,21]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-0609.2000.9r200.x"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(90)91388-Q"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.pupt.2004.09.030"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1007\/s001099900073"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2362.2000.00736.x"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bmt.1702387"},{"key":"e_1_2_6_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bmt.1705969"},{"key":"e_1_2_6_9_2","doi-asserted-by":"publisher","DOI":"10.1002\/j.1460-2075.1991.tb07761.x"},{"key":"e_1_2_6_10_2","doi-asserted-by":"publisher","DOI":"10.1080\/08923970701692577"},{"key":"e_1_2_6_11_2","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000043924.09647.61"},{"key":"e_1_2_6_12_2","doi-asserted-by":"crossref","first-page":"2569","DOI":"10.4049\/jimmunol.162.5.2569","article-title":"N\u2010acetyl\u2010L\u2010cysteine inhibits primary human T cell responses at the dendritic cell level: association with NF\u2010kappaB inhibition","volume":"162","author":"Verhasselt V.","year":"1999","journal-title":"J. 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