title: CD69, HLA-DR and the IL-2R identify persistently activated T cells in psoriasis vulgaris lesional skin: blood and skin comparisons by flow cytometry.
abstract: Many lymphocyte-activation-associated molecules are observed by immunohistochemistry in psoriasis vulgaris lesional skin. Non-T cells in lesional skin also express these molecules. We quantitatively measured the number of T cells expressing cell surface activation-associated molecules (CD69, CD25, CD122, HLA-DR) and co-stimulatory molecules (CD28, CTLA-4, CD80, CD86), including a Type 2 T cell marker (CD30) and CD11b, by flow cytometry of skin and peripheral blood. T cells in single cell suspensions of psoriatic lesional-epidermis-expressed HLA-DR (86%), CD69 (59%), CD25 (55%), CD122 (44%), and CD28 (91%). Dermal T cells showed similar percentages except for CD69 (17%). CD69 was found directly in lesional skin biopsies by immunohistochemistry. Both CD4 and CD8 subsets from lesional skin contained large populations of CD25+ cells with a bias towards CD8 activation in the epidermis and towards CD4 activation in the dermis. CD86, CD80, CTLA-4, CD30 and CD11b were expressed by less than 23% of the T cell populations from both the epidermis and dermis. CD30+CD4+ cells were found two-fold over CD8+ T cells. These results show that the majority of lesional lymphocytes are persistently activated. We also found the majority of Type 2 associated markers primarily on the CD4+ epidermal T cell population. Psoriatic blood contained elevated levels of T cells expressing CD25, primarily within the CD8+ subset. Thus the majority of lesional T cells expressed the three primary activation markers, while psoriatic blood T cells were distinguished by an increase in CD25, specifically within the CTL population.
authors.affiliation: Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10021, USA.
authors.forename: K
authors.initials: K
authors.lastname: Ferenczi
authors.forename: L
authors.initials: L
authors.lastname: Burack
authors.forename: M
authors.initials: M
authors.lastname: Pope
authors.forename: J G
authors.initials: JG
authors.lastname: Krueger
authors.forename: L M
authors.initials: LM
authors.lastname: Austin
mesh_terms: D000069594:Abatacept; D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism*; D000943:Antigens, Differentiation / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism*; D015551:Autoimmunity; D018122:B7-1 Antigen / Q000378:metabolism; D051940:B7-2 Antigen; D015415:Biomarkers; D018106:CD28 Antigens / Q000378:metabolism; D016516:CD4-CD8 Ratio; D060908:CTLA-4 Antigen; D005260:Female; D006684:HLA-DR Antigens / Q000378:metabolism*; D006801:Humans; D018796:Immunoconjugates; D017730:Ki-1 Antigen / Q000378:metabolism; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D016177:Macrophage-1 Antigen / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D008875:Middle Aged; D011565:Psoriasis / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D015375:Receptors, Interleukin-2 / Q000378:metabolism*; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D000099192:CD69 Antigens
chemical_list: D000069594:Abatacept; D015703:Antigens, CD; D000943:Antigens, Differentiation; D000945:Antigens, Differentiation, T-Lymphocyte; D018122:B7-1 Antigen; D051940:B7-2 Antigen; D015415:Biomarkers; D018106:CD28 Antigens; D060908:CTLA-4 Antigen; D006684:HLA-DR Antigens; D018796:Immunoconjugates; D017730:Ki-1 Antigen; D037181:Lectins, C-Type; D016177:Macrophage-1 Antigen; D008562:Membrane Glycoproteins; D015375:Receptors, Interleukin-2; D000099192:CD69 Antigens; C497964:CD86 protein, human; C556706:CTLA4 protein, human