Document 0609
 DOCN  M9650609
 TI    Suppression of cytokine production in T helper type 2 cells by nitric
       oxide in comparison with T helper type 1 cells.
 DT    9605
 AU    Nukaya I; Takagi K; Kawabe T; Suketa Y; Department of Environmental
       Biochemistry, School of; Pharmaceutical Science, University of Shizuoka,
       Japan.
 SO    Microbiol Immunol. 1995;39(9):709-14. Unique Identifier : AIDSLINE
       MED/96123367
 AB    We examined the effect of nitric oxide (NO) on cytokine production in T
       helper (Th) cell subsets, using murine splenic CD4+ T cells and two
       types of Th clones. Interferon-gamma-treated murine peritoneal exudate
       cells (IFN-PEC) suppressed DNA synthesis to 60% of the control level in
       CD4+ T cells stimulated with the anti-CD3 monoclonal antibody. The
       production of IL-2 and IL-4 in the CD4+ T cells decreased to 63.2% and
       9.2%, respectively, of the control value by co-culture with IFN-PEC. The
       addition of NG-monomethyl-L-arginine (L-NMMA) partially recovered the
       suppression of DNA synthesis. In the presence of indomethacin, the
       suppression of DNA synthesis was partially inhibited and the reduction
       in the cytokine production caused by IFN-PEC was partially recovered.
       The simultaneous addition of NG-monomethyl-L-arginine (L-NMMA) and
       indomethacin completely inhibited not only the suppression of DNA
       synthesis but also the reduction in the cytokine production caused by
       IFN-PEC. Moreover, DNA synthesis in the Th2 clone was suppressed to a
       greater extent than that in the Th1 clone by co-culture with IFN-PEC.
       This suppression in the Th1 clone was inhibited by the addition of
       L-NMMA, whereas the DNA synthesis in the Th2 clone was not recovered by
       L-NMMA. In addition, sodium nitroprusside (SNP) suppressed IL-4
       production in the Th2 clone but had no effect on IL-2 production in the
       Th1 clone. In the experiment of the co-culture with IFN-PEC, the
       inhibitory-effect of NO on T cell activation was not clarified by the
       influence of prostaglandins. However, in conclusion, cytokine production
       in Th2 cells may be more susceptible to NO than that in Th1 cells.
 DE    Animal  Anti-Inflammatory Agents, Non-Steroidal/PHARMACOLOGY
       Arginine/ANALOGS & DERIVATIVES/PHARMACOLOGY  Cell Line  Cells, Cultured
       Comparative Study  Cytokines/*BIOSYNTHESIS  CD4-Positive
       T-Lymphocytes/DRUG EFFECTS/METABOLISM  Drug Combinations
       DNA/BIOSYNTHESIS  DNA Replication/DRUG EFFECTS  Enzyme
       Inhibitors/PHARMACOLOGY  Female  Indomethacin/PHARMACOLOGY  Interferon
       Type II/PHARMACOLOGY  Mice  Mice, Inbred BALB C  Mice, Inbred C3H
       Nitric Oxide/*PHARMACOLOGY  Nitric-Oxide Synthase/ANTAGONISTS & INHIB
       Nitroprusside/PHARMACOLOGY  Spleen/CYTOLOGY  Th1 Cells/DRUG
       EFFECTS/*METABOLISM  Th2 Cells/DRUG EFFECTS/*METABOLISM  JOURNAL ARTICLE

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