PHENOTYPIC AND FUNCTIONAL CELLULAR DIFFERENCES BETWEEN HUMAN CD3(-) DECIDUAL AND PERIPHERAL-BLOOD LEUKOCYTES


DENİZ G., CHRISTMAS S., BREW R., JOHNSON P.

JOURNAL OF IMMUNOLOGY, cilt.152, sa.9, ss.4255-4261, 1994 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 152 Sayı: 9
  • Basım Tarihi: 1994
  • Dergi Adı: JOURNAL OF IMMUNOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.4255-4261
  • İstanbul Üniversitesi Adresli: Hayır

Özet

CD3(-) leukocyte clones derived from human decidualized endometrial tissue of first trimester pregnancy have been compared with CD3(-) PBL clones. Most CD3(-) decidual granulated leukocyte (DGL) clones were CD16(-) CD56(+) whereas most CD3(-) PBL clones were CD16(+) CD56(+). CD3(-) DGL and PBL clones, whether CD16(+) or not, showed MHC-nonrestricted NK cell activity. However, CD3(-) CD16(-) DGL clones had low cytotoxic activity against the NK-resistant cell line BSM, whereas CD3(-) CD16(+) DGL and CD3(-) PBL clones were strongly cytotoxic. Cytolytic activity has also been investigated in respect of target cell HLA-G expression, because this nonpolymorphic class I MHC molecule is expressed selectively by invasive fetal cytotrophoblast. Class I HLA Ag loss cell mutants were killed efficiently by CD3(-) DGL clones. Expression of transfected HLA-B8 increased their sensitivity to lysis by most CD3(-) DGL clones, whereas expression of transfected HLA-G commonly led to decreased target cell killing. In addition, the effects of uncloned CD3(-) DCL on the one-way MLR have been examined. These cells were very poor responders and, unless cultured to induce expression of class II MHC molecules, were also very poor stimulators. When fresh CD3(-) DGLs were added as third-party cells, either autologous or allogeneic to responder cells, [H-3]TdR incorporation was decreased in the MLR. Thus, CD3(-) DGL clones express MHC-nonrestricted cytolytic activity, notably against HLA-negative cells, but expression of HLA-G offers protection to target cells. In addition, CD3(-) DGL may function to suppress allogeneic responses.