TRANSFORMATION OF LYMPHOCYTE-T SUBSETS BY MAREKS-DISEASE HERPESVIRUS

被引:123
作者
SCHAT, KA [1 ]
CHEN, CLH [1 ]
CALNEK, BW [1 ]
CHAR, D [1 ]
机构
[1] UNIV ALABAMA, CTR COMPREHENS CANC, DEPT MICROBIOL, BIRMINGHAM, AL 35294 USA
关键词
D O I
10.1128/JVI.65.3.1408-1413.1991
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Marek's disease herpesvirus (MDV)-transformed lymphoblastoid tumor cell lines were characterized for the presence of the surface markers. Monoclonal antibodies were used for CD3 (T-cell receptor [TCR] complex), TCR1, TCR2, and TCR3, CD4, CD8, and Ia antigen by indirect fluorescence staining followed by microscopic examination or flow cytometry. The lymphoblastoid cell lines were obtained from tumors from chickens infected with MDV (n = 44) or from local lesions induced by inoculation of allogeneic, MDV-infected chick kidney cells (n = 56). Lymphocytes were harvested from these lesions between 4 and 16 days postinoculation and cultured in vitro to establish cell lines. All cell lines expressed Ia antigen and CD3 and/or TCR and thus are activated T cells. Most of the cell lines developed from tumors were CD4+ CD8-; only one cell line was negative for both markers. Sixteen percent of the cell lines were TCR3+, while the remainder were TCR2+. The cell lines developed from local lesions were much more heterogeneous: 45% were CD4- CD8+, 34% were CD4- CD8-, and only 21% were CD4+ CD8-. The number of TCR3+ cell lines was larger than expected for the CD4- CD8+ and CD4- CD8- cell lines, as judged from the presence of these cells in the blood. These results indicate that several subsets of T lymphocytes can be transformed by MDV, depending on the pathogenesis of infection. Activation of T cells as a consequence of the normal pathogenesis or by allogeneic stimulation seem to be a first important step in the process of transformation.
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页码:1408 / 1413
页数:6
相关论文
共 50 条
[1]  
ABPLANALP H, 1985, INT S MAREKS DISEASE, P347
[2]  
AKIYAMA Y, 1974, BIKEN J, V17, P105
[3]   QUICK-BLOT - SELECTIVE MESSENGER-RNA OR DNA IMMOBILIZATION FROM WHOLE CELLS [J].
BRESSER, J ;
DOERING, J ;
GILLESPIE, D .
DNA-A JOURNAL OF MOLECULAR & CELLULAR BIOLOGY, 1983, 2 (03) :243-254
[4]  
BROGREN CH, 1981, IMMUNOBIOLOGY, V159, P65
[5]  
BUCY RP, 1990, J IMMUNOL, V144, P1161
[6]   PRODUCTION OF AN IMMUNE SUPPRESSOR FACTOR BY MAREKS-DISEASE LYMPHOBLASTOID CELL-LINES [J].
BUMSTEAD, JM ;
PAYNE, LN .
VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY, 1987, 16 (1-2) :47-66
[7]   EFFECT OF IMMUNOCOMPETENCE ON THE ESTABLISHMENT AND MAINTENANCE OF LATENCY WITH MAREKS-DISEASE HERPESVIRUS [J].
BUSCAGLIA, C ;
CALNEK, BW ;
SCHAT, KA .
JOURNAL OF GENERAL VIROLOGY, 1988, 69 :1067-1077
[8]  
CABALLERO A, 1989, J IMMUNOGENET, V16, P321
[9]   INFLUENCE OF AGE AT EXPOSURE ON PATHOGENESIS OF MAREKS-DISEASE [J].
CALNEK, BW .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1973, 51 (03) :929-939
[10]   PATHOGENESIS OF MAREK DISEASE VIRUS-INDUCED LOCAL LESIONS .1. LESION CHARACTERIZATION AND CELL-LINE ESTABLISHMENT [J].
CALNEK, BW ;
LUCIO, B ;
SCHAT, KA ;
LILLEHOJ, HS .
AVIAN DISEASES, 1989, 33 (02) :291-302