Document 0196
 DOCN  M9440196
 TI    Induction of HLA class I and class II expression in human T-lymphotropic
       virus type I-infected neuroblastoma cells.
 DT    9404
 AU    Lehky TJ; Cowan EP; Lampson LA; Jacobson S; Neuroimmunology Branch,
       NINDS, NIH, Bethesda, MD 20892.
 SO    J Virol. 1994 Mar;68(3):1854-63. Unique Identifier : AIDSLINE
       MED/94149881
 AB    Human T-lymphotropic virus type I (HTLV-I) is associated with a
       neurologic disease, HTLV-I-associated myelopathy-tropical spastic
       paraparesis, in which both pathological and immunological changes are
       observed within the central nervous system. The pathogenesis of
       infection in HTLV-I-associated myopathy-tropical spastic paraparesis is
       not well understood with respect to the cell tropism of HTLV-I and its
       relationship to the destruction of neural elements. In this study,
       neuroblastoma cells were infected with HTLV-I by coculturing with
       HUT-102 cells to demonstrate that cells of neuronal origin are
       susceptible to this retroviral infection. HTLV-I infection of the
       neuroblastoma cells was confirmed by verifying the presence of HTLV-I
       gp46 surface antigens by flow cytometry and by verifying the presence of
       HTLV-I pX RNA by Northern (RNA) blotting and in situ hybridization
       techniques. To determine whether HTLV-I infection could potentially lead
       to changes in cell surface recognition by the immune system, the
       infected neuroblastoma cells were analyzed for altered HLA expression.
       The HTLV-I-infected, cocultured neuroblastoma cells were shown, through
       cell surface antigen expression and RNA transcripts, to express HLA
       classes I and II. In contrast, cocultured neuroblastoma cells that did
       not become infected with HTLV-I expressed only HLA class I. HLA class I
       expression was enhanced by the cytokines tumor necrosis factor alpha and
       gamma interferon and in the presence of HUT-102 supernatant. In this
       system, expression of HLA class I and II molecules appeared to be
       regulated by different mechanisms. HLA class I expression was probably
       induced by cytokines present in the HUT-102 supernatant and was not
       dependent on HTLV-I infection. HLA class II expression required HTLV-I
       infection of the cells. The observation of HTLV-I infection leading to
       HLA induction in these neuroblastoma cells provides a possible mechanism
       for immunologic recognition of infected neuronal cells.
 DE    Cell Communication  Cytokines/PHARMACOLOGY  *Gene Expression
       Regulation/DRUG EFFECTS  Gene Products, env/BIOSYNTHESIS
       Histocompatibility Antigens Class I/*BIOSYNTHESIS/GENETICS
       Histocompatibility Antigens Class II/*BIOSYNTHESIS/GENETICS  Human  HTLV
       Antigens/BIOSYNTHESIS/ISOLATION & PURIF  HTLV-I/*IMMUNOLOGY  In Situ
       Hybridization  Neuroblastoma/IMMUNOLOGY/MICROBIOLOGY
       Neurons/*IMMUNOLOGY/*MICROBIOLOGY  Retroviridae Proteins,
       Oncogenic/BIOSYNTHESIS  RNA, Messenger/ANALYSIS  RNA, Viral/ISOLATION &
       PURIF  Sympathetic Nervous System/IMMUNOLOGY/MICROBIOLOGY  Tumor Cells,
       Cultured/IMMUNOLOGY/MICROBIOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).