title: Analysis of T-lymphocyte subsets after phytohemagglutinin stimulation in normal and type 1 diabetic mothers and their infants.
abstract: OBJECTIVE
  Our aim was to investigate the immunological status of diabetic pregnancy, which is an overlap of diabetic immunity abnormalities and the immunological modifications normally occurring during pregnancy.
  
  
  METHODS
  We studied lymphocyte subpopulations and lymphokine production, after 96 h of phytohemagglutinin (PHA) stimulation, from normal and Type I diabetic pregnant women at delivery time and from the respective cord blood.
  
  
  RESULTS
  Peripheral blood mononuclear cells (PBMC) from both normal and Type I diabetic mothers showed an increase in CD8+ and a decrease in CD4+ cells compared to the respective cord blood mononuclear cells (CBMC). Moreover, Type I PBMC showed a lower number of "activated" CD3+ DR+ cells and a higher number of CD8+ CD25+ cells with respect to normal women, which may reflect the dysregulatory pattern due to the autoimmune condition. Type I CBMC showed a big increase in the number of CD4+ Leu8+ cells, a cell subpopulation characterized by inhibitory activity. Finally, as regards lymphokine release in culture supernatants, type I diabetes seemed to be associated with an over-production of IL1 and IL6, although the latter increase is less evident in CBMC cultures.
  
  
  CONCLUSIONS
  The present study shows that diabetic pregnancy is associated with major alterations of cell-mediated immunity leading to a state of immunodepression. Moreover, our study suggests that the maternal immunological status influences fetal immunity, as demonstrated by the increase in the number of regulatory cells and by the altered pattern of lymphokine production (IL1 and IL6) by lymphocytes derived from diabetic CBMC. The latter phenomenon perfectly mirrors maternal PBMC characteristics.
authors.affiliation: Laboratory of Immunology, University of Palermo, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Giordano
authors.forename: R
authors.initials: R
authors.lastname: De Maria
authors.forename: A
authors.initials: A
authors.lastname: Mattina
authors.forename: G
authors.initials: G
authors.lastname: Stassi
authors.forename: M
authors.initials: M
authors.lastname: Todaro
authors.forename: A
authors.initials: A
authors.lastname: Pugliese
authors.forename: G
authors.initials: G
authors.lastname: Galluzzo
authors.forename: R M
authors.initials: RM
authors.lastname: Botta
authors.forename: A
authors.initials: A
authors.lastname: Galluzzo
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D002478:Cells, Cultured; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D005260:Female; D005312:Fetal Blood / Q000276:immunology*; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D007111:Immunity, Cellular; D007371:Interferon-gamma / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000276:immunology*; D010835:Phytohemagglutinins / Q000494:pharmacology; D011247:Pregnancy / Q000276:immunology*; D011254:Pregnancy in Diabetics / Q000276:immunology*; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D015703:Antigens, CD; D006684:HLA-DR Antigens; D007375:Interleukin-1; D007376:Interleukin-2; D015850:Interleukin-6; D010835:Phytohemagglutinins; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma