Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021345 (infectious mononucleosis)
 3,358 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peripheral T-lymphocytes from patients with infectious mononucleosis are cytotoxic towards target cells from Epstein-Barr virus-genome carrying human lumphoblastoid lines. Thus, these T-cells appear to be sensitized to viral coded determinants. Daudi cells, that carry EBV-genome, but lack HLA antigens are resistant to specific cytolysis in this model. These results suggest direct HLA involvement in the target structure recognized by birus-sensitized cytolytic T-lymphocytes in human.
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PMID:[Cytotoxicity of human T-lymphocytes sensitized by Epstein-Barr virus. Role of HLA antigens at the surface of target cells infected by the virus]. 19 80

The beta2-microglobulin/HLA deficient Burkitt lymphoma line Daudi was tested for sensitivity to EBV-specific cytotoxicity mediated by natural killer (NK)-depleted T-cells from acute mononucleosis patients. While the Daudi line was not as sensitive as the reference EBV-genome-positive target line, it was clearly sensitive in the majority of cases. This would speak against a major role of syngeneic restriction in this system.
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PMID:The EBV-carrying, beta2M/HLA deficient Burkitt lymphoma line Daudi is sensitive to EBV-specific killer T-cells of mononucleosis patients. 22 36

Peripheral T lymphocytes from patients with infectious mononucleosis (IM) are sensitized in vivo against the Epstein-Barr virus (EBV). The expression of HLA-A, B, or C molecules at the target cell surface is necessary for the cytotoxic reaction because (a) EBV-positive Daudi cells lacking HLA-A, B, and C determinants are resistant to anti-EBV T-cell lysis, (b) cytolysis of EBV-positive target cells can be consistently inhibited by anti-HLA-A, B, and C and anti-beta 2 microglobulin antibodies. However, no evidence for allogeneic restriction in this system was apparent as (a) cytotoxic T lymphocytes (CTL) from one given individual could exert a cytotoxicity of a similar magnitude on different EBV-positive target cells, regardless of the number of HLA-A or B specificities shared by the effectors and targets; (b) CTL from IM patients were able to kill target cells without any HLA-A or B antigen in common; and (c) T5-1 variants lacking one or two HLA antigens at the A, B, or D locus are killed to the same extent as the parental cells. 7 of the 9 IM patients with detectable circulating anti-EBV CTL carried the HLA-A1 antigen, whereas none of the 16 IM patients lacking detectable peripheral CTL were HLA-A1 positive (mean specific lysis of T5-1 target cells by T cells from HLA-A1 positive patients: 29.3 vs. 0.6% in HLA-A1-negative patients) (P less than 10(-9)). These data suggest an HLA-A1-linked gene control of the magnitude of the anti-EBV CTL response. Thus, the HLA region appears to act at two different level sin the T-cell-mediated lysis of EBV-infected cells by controlling first, the development of anti-EBV and second, the expression of HLA-A, B, and C molecules involved as recognition structures at the target cell surface.
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PMID:Absence of allogeneic restriction in human T-cell-mediated cytotoxicity to Epstein-Barr virus-infected target cells. Demonstration of an HLA-linked control at the effector level. 22 86

Mononuclear peripheral blood lymphocytes (PBL) from patient with infectious mononucleosis (IM) were tested in a 51Cr-release assay for cytotoxicity against autologous and allogeneic lymphoblastoid cell line (LCL), or Epstein-Barr virus (EBV)-genome positive and negative cell line. In acute phase, PBL lyse an autologous LCL as well as allogeneic LCL (Wa cells). High levels of cytotoxicity were observed in the combinations between effector and target cells sharing HLA-Class 1 product. EBV-genome positive Daudi and Raji cells which lack HLA-Class 1 antigen and have mismactched HLA-Class 1 antigen, respectively showed resistance to killing. EBV-genome negative tumor cells except NK sensitive K562 cells were not killed by IM lymphocytes. However, the IM lymphocytes without atypical form in convalescent phase failed to show killing activity against autologous and allogeneic LCL. These findings suggest that cell surface membrane antigen structure on EBV-infected LCL may be able to explain the recognition and triggering of lysis of target cells by HLA-Class 1 restricted cytotoxic T cells (CTL) from acute IM. Phenotypic analysis of PBL with atypical form from IM was made by two-color flow cytometry. The data demonstrate that CD8+ T cells quantitatively represent the major population of lymphocytes expanded during acute IM. Furthermore, approximately 70% of these CD8+ T cells express HLA-DR on these surface, suggesting that they have undergone activation. However, IL 2R (CD25 antigen) expression was not significantly elevated on activated T cells. The salient profile on cytofluorographs of an acute IM was the increased number of CD3+CD19-, CD8+CD11b-, CD8+CD28+ and CD8+S6F1+ cells. However, CD3-CD19+, CD8+CD11b+, CD8+S6F1-, CD4+Leu8- and CD25+HLA-DR+ antigens were little expressed. Increased number of CD8+CD11b-, CD8+CD28+ and CD8+S6F1+ cells, which are regarded as CTL were reduced according to the improvement of the clinical symptoms and laboratory findings. These results together with HLA typing analysis suggested a possibility HLA-Class 1 restriction of the CTL with surface phenotype of CD8+CD11b-, CD8+CD28+, and CD8+S6F1+.
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PMID:CD8+ T cell subsets of cytotoxic T lymphocytes induced by Epstein-Barr virus infection in infectious mononucleosis. 196 52

The Epstein-Barr virus-determined nuclear antigen (EBNA) is the only known virally-determined component that is regularly associated with EBV-transformed cells. A main component of EBNA, herein designated EBNA-1, has been conclusively localized to the BamHI K fragment of the viral genome. EBNA-1 is present in all EBV-carrying cell lines so far studied. Our current study deals with a second component. We have found that the EBNA reaction detected by anti-complement immunofluorescence (ACIF) in Burkitt lymphoma lines Daudi, Jijoye, and P3HR-1 could be completely removed by preabsorption of sera with any one of these 3 lines, when tested against any other of them. The same absorbed sera still gave a brilliant nuclear staining against other EBV-carrying lines, e.g. Raji or B95-8. The 3 lines in the first category carry EBV genomes that have deletions in the BamHI WYH region of the EBV genome. This region is intact in the second group of lines. This result is interpreted as showing the existence of 2 different ACIF-stainable EBV-determined nuclear antigens, one of which is associated with the BamHI WYH region. We designate this antigen as EBNA-2. We found that the two different EBNAs are different with regard to their association with metaphase chromosomes. In lines positive for both EBNA subtypes, metaphase chromosomes gave brilliant EBNA-1 staining, but could not be stained for EBNA-2, indicating differences in chromatin association of the two EBNAs. An 86 kd polypeptide was identified by immunoblotting of DNA-binding proteins from EBV-transformed lymphoid cell lines. EBV-specificity of the polypeptide was demonstrated by the presence of antibodies against this polypeptide in antisera from a population of EBV-seropositive donors, but not from seronegative donors, by the presence of the polypeptide itself in EBV-carrying but not in EBV-negative cell lines and by the appearance of antibodies against this polypeptide during the course of infectious mononucleosis (IM). The polypeptide was absent from the EBV-carrying P3HR-1, Daudi and Jijoye cell lines, which suggested that it may be encoded by the BamHI WYH region that is deleted from the viral substrains carried by these lines.
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PMID:Characterization of a second Epstein-Barr virus-determined nuclear antigen associated with the BamHI WYH region of EBV DNA. 298 49

Patients with seropositive rheumatoid arthritis (RA) have elevated titers of precipitating antibody toward an antigen designated RA nuclear antigen (RANA). Anti-RANA reactivity has been associated with prior Epstein-Barr virus (EBV) infection. Using the protein blot technique, we have identified, in extracts of WI-L2, an EBV+ nonproducer B-lymphoblast line, a Mr 80,000 polypeptide that is reactive with anti-RANA-containing sera. This same polypeptide can be recovered from RANA precipitin bands. The Mr 80,000 polypeptide appears to be EBV-associated, as a homologous antigen was detected in two other EBV+ cell lines, Daudi and Raji, but was not present in three EBV- human cell lines tested, HeLa, BJAB, and Ramos. Anti-RANA antibodies and antibodies reactive with the Mr 80,000 polypeptide also appear coincidently in the sera of individuals exhibiting an EBV infection (infectious mononucleosis). Further analysis of the RANA-associated Mr 80,000 polypeptide suggested its identity with the previously recognized EBV-associated nuclear antigen designated EBNA. The Mr 80,000 antigen shares with EBNA the properties of being a heat-stable, DNA binding protein. EBNA is traditionally assayed by a complement fixation reaction and anti-Mr 80,000 antibodies were shown to be reactive when a complement fixation assay was used in the immunoblot. Finally, when the Mr 80,000 antigen was used to absorb an anti-RANA/anti-EBNA serum, both antibodies were reduced.
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PMID:Antibodies to the Epstein-Barr virus nuclear antigen and to rheumatoid arthritis nuclear antigen identify the same polypeptide. 631 43