title: Lack of correlation between membrane CD30 expression and cytokine secretion pattern in allergen-primed naive cord blood T-cell lines and clones.
abstract: Various surface molecules are expressed by activated T cells. Among them, the CD30 antigen has been proposed as a reproducible marker that identifies a subset of differentiated and/or activated T lymphocytes that produce T helper (Th)-2-type cytokines, i.e. interleukin (IL)-4 and IL-5. However, because CD30 has mainly been detected on established T-cell clones, it is still unclear whether a priming allergen and/or cytokine can induce its membrane expression on naive T cells, perhaps in parallel with the up-regulation of other relevant activation markers, such as CD25, HLA-DR and L-selectin. It is also unknown whether proper allergen stimulation affects the cytokine secretion pattern by CD30+ T-cell clones derived from antigen-unprimed (naive) T lymphocytes. More information on these questions was sought by adopting a model that used cord blood as a source of virgin T cells and exposing them to native cypress allergen or cytokine (IL-2 or IL-4) stimulation, as well as to conventional polyclonal activators such as PHA or anti-CD3. Peripheral blood MC from four adult cypress-sensitive patients was also assayed and used as controls for all culture experiments. Freshly isolated cord and adult T cells did not express the CD30 antigen on their membrane. Many of the stimulating agents tested were able to up-regulate the expression of CD30. However, despite high expression of this molecule, cloned allergen-specific cord CD4+ T lymphocytes were unable to produce IFN-gamma and/or IL-4. In contrast, they retained the capability to produce IL-2. Thus, expression of the CD30 antigen on virgin T cells does not correlate with a polarized model of T helper (Th)-1 or Th-2 cytokine-producing cells, suggesting that these types of lymphokine-secreting lymphocytes are not a paradigmatic example of T-cell subpopulations that display stable phenotypical features.
authors.affiliation: Department of Internal Medicine, University of Perugia School of Medicine, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Spinozzi
authors.forename: E
authors.initials: E
authors.lastname: Agea
authors.forename: S
authors.initials: S
authors.lastname: Piattoni
authors.forename: B
authors.initials: B
authors.lastname: Falini
authors.forename: F
authors.initials: F
authors.lastname: Grignani
authors.forename: A
authors.initials: A
authors.lastname: Bertotto
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D002460:Cell Line; D002999:Clone Cells; D016207:Cytokines / Q000378:metabolism*; D005312:Fetal Blood / Q000276:immunology*; D006801:Humans; D007114:Immunization; D016130:Immunophenotyping; D017730:Ki-1 Antigen / Q000096:biosynthesis*; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D008213:Lymphocyte Activation; D016176:T-Lymphocyte Subsets / Q000145:classification / Q000276:immunology* / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology / Q000378:metabolism
chemical_list: D000485:Allergens; D016207:Cytokines; D017730:Ki-1 Antigen