title: Decreased CD7 expression in cutaneous infiltrates of HIV-1+ patients. Military Medical Consortium for the Advancement of Retroviral Research (MMCARR).
abstract: CD7 is an early T-cell marker that has been used in the diagnosis of stem cell leukemias. Loss of expression of CD7 with a battery of other mature T-cell markers has also been used as one criteria in the diagnosis cutaneous T-cell lymphomas. More recently, CD7-negative T cells have been shown to be a normal population of T cells in the peripheral blood and the skin, and may represent a mature T-cell population with a different pattern of maturation and activation. In addition, in HIV-1 disease expansion of CD7-negative T cells has been found in the peripheral blood. We evaluated the number of CD7-negative T cells in skin infiltrates to determine whether there was an increase of CD7-negative T cells. We studied T-cell markers including CD3, CD4, CD7, CD8, CD20, CD29, and HLA-DR on cutaneous biopsy material from inflammatory dermatoses in 57 patients with HIV-1 disease in Walter Reed stages (WR) 1-6, and in 14 HIV-1-negative patients WR0. The inflammatory infiltrates showed a moderate to marked decrease in CD7 expression on CD3+ T cells in benign inflammatory infiltrates of the majority of HIV-1+ patients. The majority of HIV-1-negative patients showed no decrease in CD7 expression, although 5 of 14 showed a moderate decrease and 1 of 14 showed a marked decrease. Although the nature of CD7- T cells has not been clearly defined, this population of mature T cells appears to have distinct immunologic properties as well as a trophism for skin. Better characterization of these T cells, as well as factors that promote their maturation and activation, may give clues to the high incidence as well as the pathogenesis of skin disease in HIV-1+ patients.
authors.affiliation: United States Army Medical Research Institute for Chemical Defense, Aberdeen, MD, USA.
authors.forename: K J
authors.initials: KJ
authors.lastname: Smith
authors.forename: H G
authors.initials: HG
authors.lastname: Skelton
authors.forename: W S
authors.initials: WS
authors.lastname: Chu
authors.forename: J
authors.initials: J
authors.lastname: Yeager
authors.forename: P
authors.initials: P
authors.lastname: Angritt
authors.forename: K F
authors.initials: KF
authors.lastname: Wagner
mesh_terms: D018951:Antigens, CD20 / Q000032:analysis / Q000235:genetics; D019011:Antigens, CD7 / Q000032:analysis / Q000235:genetics*; D017252:CD3 Complex / Q000032:analysis / Q000235:genetics; D015704:CD4 Antigens / Q000032:analysis / Q000235:genetics; D016827:CD8 Antigens / Q000032:analysis / Q000235:genetics; D005786:Gene Expression Regulation; D018023:HIV Seronegativity; D006679:HIV Seropositivity / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D015497:HIV-1 / Q000276:immunology*; D006684:HLA-DR Antigens / Q000032:analysis / Q000235:genetics; D006801:Humans; D019012:Integrin beta1 / Q000032:analysis / Q000235:genetics; D008213:Lymphocyte Activation / Q000276:immunology; D018655:Lymphocyte Count; D017193:Skin Diseases, Viral / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology
chemical_list: D018951:Antigens, CD20; D019011:Antigens, CD7; D017252:CD3 Complex; D015704:CD4 Antigens; D016827:CD8 Antigens; D006684:HLA-DR Antigens; D019012:Integrin beta1