2005 Fiscal Year Final Research Report Summary
analysis of host-immune responses to the EB virus-associated skin disorders
| Project/Area Number |
16591099
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
TSUJI Kazuhide OKAYAMA UNIVERSITY, HOSPITAL of MEDICINE and DENTISTRY, lecturer, 医学部・歯学部附属病院, 助手 (30304356)
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| Co-Investigator(Kenkyū-buntansha) |
IWATSUKI Keiji OKAYAMA UNIVERSITY, GRADUATE SCHOOL of MEDICINE, DENTISTRY and PHARMACEUTICAL SCIENCES, M.D., PhD., Professor, 大学院・医歯薬学総合研究科, 教授 (80126797)
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| Project Period (FY) |
2004 – 2005
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| Keywords | EB virus / peptide / tumor immunology / Chronic EB virus infection / CTL |
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| Research Abstract |
We have shown that cutaneous disorders such as hydroa vacciniforme (HV) and hypersensitivity to mosquito bites (HMB) are mediated by Epstein-Barr (EBV)-infected T and NK cells, respectively. Patients with HV-like lymphomas and other EBV-associated NK/T-cell lymphoproliferative disorder (LPD) with poor prognosis occur preferentially in our country. Patients with cutaneous lesions of EBV-associated NK/T-cell LPD were enrolled in the present study and we analyzed the clinical and pathological conditions of these patients. For the purpose of detection of latently-infected EBV, we tried to detect the EBV genome by PCR, the viral antigens by immunostaining and the gene transcripts in the tissue by in situ hybridization. Clonal expansion of the same EBV episome were detected by southern blotting assay. Several Epstein-Barr virus (EBV)-carrying CD56+ lines were established from peripheral blood lymphocytes (PBL) of patients with severe chronic active EBV infection, in the presence of interleukin-2. All lines carried EBV genomes in a single episomal form. All lines expressed EBV-encoded small RNA (EBER) 1, nuclear antigen (EBNA) 1, and latent membrane protein (LMP). Cytotoxic T lymphocyte (CTL) responses of patients against EBV-infected cells were confirmed. However, EBV-carrying CD56+ cell-mediated cytolytic activity was defective. The secretion of certain cytokines known to be important in initiating antiviral immune responses was markedly reduced in the CD56+ cell subset. These data suggest that the expansion of this highly dysfunctional CD56+ cell subset in EBV-associated LPD individuals may account for the impaired function of the total NK cell population.
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Research Products
(12 results)
