Identification of Genes Involved in the Suppression of Antibody Production from Human Peripheral Blood Lymphocytes

  • AIBA Yoshihiro
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University
  • YAMASHITA Makiko
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University
  • KATAKURA Yoshinori
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University
  • FURUKAWA Yuki
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University
  • MATSUMOTO Shin-ei
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University
  • TOMIMATSU Kousuke
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University
  • TERUYA Kiichiro
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University
  • SHIRAHATA Sanetaka
    Graduate School of Systems Life Sciences, Faculty of Agriculture, Kyushu University Department of Genetic Resources Technology, Faculty of Agriculture, Kyushu University

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抄録

Pretreatment with L-leucyl-L-leucine methyl ester (LLME) is a prerequisite for peripheral blood mononuclear cells (PBMCs) to produce antigen-specific antibodies when sensitized with an antigen. Little information, however, is available regarding the mechanisms involved in LLME-induced augmentation of antibody production from PBMCs that are antigen sensitized. In the present study, we attempted to identify the genes involved in the suppression of antibody production from PBMCs that was not treated with LLME, but sensitized with an antigen. Using subtractive screening, we obtained 63 independent genes, including 17 EST genes, that are specific for LLME-nontreated PBMC. Among these genes, the expression of heavy chain ferritin (H-ferritin), CC chemokine ligand 18 (CCL18), and matrix metalloproteinase 12 (MMP12) were augmented in LLME-nontreated PBMCs, suggesting that inflammatory factors might be involved in the suppression of antibody production in LLME-nontreated PBMCs.

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