Phenotypes of B Cells Differ in EBV-positive Burkitt-s lymphoma Derived Cell Lines

Epstein-Barr virus (EBV) is implicated in the pathogenesis of the endemic Burkitt-s lymphoma (BL). The EBVpositive BL-derived cell lines initially maintain the original tumor phenotype of EBV infection (latency I, LatI), but most of them drift toward a lymphoblast phenotype of EBV latency III (LatIII) during in vitro culturing. The aim of the present work was to characterize the B-cell subsets in EBV-positive BL cell lines and to verify whether a particular cell subset correlates with the type of EBV infection. The phenotype analysis of two EBV-negative and eleven EBV-positive (three of LatI and eight of LatIII) BL cell lines was performed by polychromatic flow cytomery, based on expression pattern of CD19, CD10, CD38, CD27, and CD5 markers. Two cell subsets, CD19+CD10+ and CD19+CD10-, were defined in LatIII BL cell lines. In both subsets, the CD27 and CD5 cell surface expression was detected in a proportion of the cells.





References:
[1] C. A. Van den Bosch, "Is endemic Burkitt's lymphoma an alliance
between three infec-tions and a tumor promoter?," Lancet Oncol., pp.
5738-5746, 2004.
[2] G. Brady, G. J. MacArthur, P. J. Farrell, "Epstein-Barr virus and Burkitt
lymphoma," J. Clin. Pathol., vol. 60(12), pp. 1397-1402, 2007.
[3] C. Bellan, L. Stefano, F. Giulia de, E. A. Rogena, L. Lorenzo, "Burkitt
lymphoma versus diffuse large B-cell lymphoma: a practical approach,"
Hematol. Oncol., vol. 28(2), pp. 53-6, 2010.
[4] U. Klein, G. Klein, B. Ehlin-Henriksson, K. Rajewsky, R. K├╝ppers,
"Burkitt's lymphoma is a malignancy of mature B cells expressing
somatically mutated V region genes," Mol. Med., vol. 1, pp. 495-505,
1995.
[5] G. Klein, "Burkitt lymphoma-a stalking horse for cancer research?,"
Semin. Cancer Biol., vol. 19(6), pp. 347-50, 2009.
[6] L. S. Young, A. B. Rickinson, "Epstein-Barr virus: 40 years on," Nat.
Rev. Cancer, vol. 4, pp. 757-768, 2004.
[7] G. Klein, E. Klein, E. Kashuba, "Interaction of Epstein-Barr virus (EBV)
with human B-lymphocytes," Biochem. Biophys. Res. Commun., vol.
396, pp. 67-73, 2010.
[8] E. Klein, L. L. Kis, G. Klein, "Epstein-Barr virus infection in humans:
from harmless to life endangering virus-lymphocyte interactions,"
Oncogene, vol. 26, pp. 1297-1305, 2007.
[9] J. Nicholas, "Human gammaherpesvirus cytokines and chemokine
receptors," J. Interferon Cytokine Res., vol. 25, pp. 373-383, 2005.
[10] T. Nakayama, R. Fujisawa, D. Izawa, K. Hieshima, K. Takada, O.
Yoshie, "Human B cells immortalized with Epstein-Barr virus
upregulate CCR6 and CCR10 and downregulate CXCR4 and CXCR5,"
J. Virol., vol. 76, pp. 3072-3077, 2002.
[11] B. Ehlin-Henriksson, W. Liang, A. Cagigi, F. Mowafi, G. Klein, A.
Nilsson, "Changes in chemokines and chemokine receptor expression on
tonsillar B cells upon Epstein-Barr virus infection," Immunology, vol.
127, pp. 549-557, 2009.
[12] D. A. Thorley-Lawson, "Epstein-Barr virus: exploiting the immune
system," Nat. Rev. Immunol., vol. 1, pp. 75-82, 2001.
[13] M. Rowe, D. T. Rowe, C. D. Gregory, L. S. Young, P. J. Farrell, H.
Rupani, A. B. Rickinson, "Dif-ferences in B cell growth phenotype
reflects novel patterns of Epstein-Barr virus latent gene expression in
Burkitt-s lymphoma cells," EMBO J., vol. 6, pp. 2743-2751, 1987.
[14] A. B. Rickinson, S. P. Lee, N. M. Steven, "Cytotoxic T lymphocyte
responses to Epstein-Barr virus," Curr. Opin. Immunol., vol. 8(4), pp.
492-497, 1996.
[15] K. Pokrovskaja, B. Ehlin-Henriksson, J. Bartkova, J. Bartek, R. Scuderi,
L. Szekely, K. G. Wiman, G. Klein, "Phenotype-related differences in
the expression of D-type cyclins in human B cell-derived lines," Cell
Growth Differ., vol. 7, pp. 1723-1732, 1996.
[16] A. Maeda, C. Kiss, F. Chen, B. Ehlin-Henriksson, N. Nagy, L. Szekely,
K. Takada, E. Klein, G. Klein, " EBNA promoter usage in EBV-negative
Burkitt lymphoma cell lines converted with a neomycin-resistant EBV
strain," Int. J. Cancer, vol. 93, pp. 714-719, 2001.
[17] I. D. Kholodnyuk, S. Kozireva, M. Kost-Alimova, V. Kashuba, G. Klein,
S. Imreh, "Down regulation of 3p genes, LTF, SLC38A3 and DRR1,
upon growth of human chromosome 3-mouse fibrosarcoma hybrids in
severe combined immunodeficiency mice," Int. J. Cancer, vol. 119, pp.
99-107, 2006.
[18] R. J. Tierney, N. Steven, L. S. Young, A. B. Rickinson, "Epstein-Barr
virus latency in blood mononuclear cells: analysis of viral gene
transcription during primary infection and in the carrier state," J. Virol.,
vol. 68, pp. 7374-7385, 1994.
[19] M. Conacher, R. Callard, K. McAulay, H. Chapel, D. Webster, D.
Kumararatne et al, "Epstein-Barr virus can establish infection in the
absence of a classical memory B-cell population," J. Virol., vol. 79, pp.
11128-11134, 2005.
[20] U. Klein, K. Rajewsky, R. K├╝ppers, "Human immunoglobulin
(Ig)M+IgD+ peripheral blood B cells expressing the CD27 cell surface
antigen carry somatically mutated variable region genes: CD27 as a
general marker for somatically mutated (memory) B cells," J. Exp. Med.,
vol. 188, pp. 1679-1689, 1998.
[21] M. Perez-Andres, B. Paiva, W. G. Nieto, A. Caraux, A. Schmitz, J.
Almeida et al, "Human peripheral blood B-cell compartments: a
crossroad in B-cell traffic," Cytometry B Clin. Cytom., vol. 78, Suppl 1,
pp. S47-60, 2010.
[22] A. Caraux, B. Klein, B. Paiva, C. Bret, A. Schmitz, G. M. Fuhler et al,
"Circulating human B and plasma cells. Age-associated changes in
counts and detailed characterization of circulating normal CD138- and
CD138+ plasma cells," Haematologica, vol. 95, pp. 1016-1020, 2010.