Article

Aberrant T cell-mediated immunity in untreated schizophrenic patients: Deficient interleukin-2 production

INSERM U25, Hôpital Necker, Paris, France.
American Journal of Psychiatry (Impact Factor: 13.56). 06/1989; 146(5):609-16.
Source: PubMed

ABSTRACT The authors examined the immune status at the cellular and humoral levels of 16 untreated schizophrenic patients. No abnormality in the distribution of T cell subsets (CD4+, CD8+) was detected. The proliferative response to the T cell mitogen phytohemagglutinin was normal. No increase in the number of T cells showing activation markers, such as human leukocyte antigens and interleukin-2 receptors, was noted. Conversely, function studies revealed a clear deficiency in interleukin-2 production by purified T cells. This lower production was probably intrinsic to the patients' T cells, since interleukin-2 production showed normal sensitivity to prostaglandin E2-mediated down-regulation by autologous monocytes.

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    • "References: 1 Barak et al. (1995); 2 Gattaz et al. (1992); 3 Xu et al. (1994); 4 Zhang et al. (2002); 5 McAllister et al. (1995); 6 Kim et al. (1998); 7 Theodoropoulou et al. (2001); 8 Maes et al. (1994); 9 Akiyama (1999); 10 Rapaport and Lohr (1994); 11 Gaughran et al. (1998); 12 Rapaport et al. (1989); 13 Haack et al. (1999); 14 Mü ller et al. (1997); 15 Erbagci et al. (2001); 16 Naudin et al. (1996); 17 Frommberger et al. (1997); 18 Ganguli et al. (1994); 19 van Kammen et al. (1999); 20 Maes et al. (1995a); 21 Baker et al. (1996); 22 Katila et al. (1994a); 23 Maes et al. (1997); 24 Katila et al. (1994b); 25 el-Mallakh et al. (1993); 26 Maes et al. (2000); 27 Maes et al. (1997); 28 Toyooka et al. (2003); 29 Rimon et al. (1985); 30 Becker et al. (1990); 31 Preble and Torrey (1985); 32 Kim et al. (2004); 33 Baker et al. (1996); 34 Kudoh et al. (2001); 35 Schattner et al. (1996); 36 Maes et al. (2002); 37 Rothermundt et al. (1998); 38 Ganguli et al. (1992); 39 Hornberg et al. (1995); 40 Bessler et al. (1995); 41 Arolt et al. (2000); 42 Ganguli et al. (1995); 43 Ganguli et al. (1989); 44 Villemain et al. (1987); 45 Yang et al. (1994); 46 Villemain et al. (1989); 47 Cazzullo et al. (2001); 48 Cazzullo et al. (1998); 49 "
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