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Tumor necrosis factor modulates CD 20 expression on cells from chronic lymphocytic leukemia: A new role for TNF alpha?
Author(s) -
Sivaraman S.,
Deshpande C.G.,
Ranganathan R.,
Huang X.,
Jajeh A.,
O'brien T.,
Huang R.W.,
Gregory S.A.,
Venugopal P.,
Preisler H.D.
Publication year - 2000
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/1097-0029(20000801)50:3<251::aid-jemt9>3.0.co;2-7
Subject(s) - cd20 , tumor necrosis factor alpha , chronic lymphocytic leukemia , autocrine signalling , cytokine , downregulation and upregulation , cancer research , medicine , immunology , monoclonal antibody , leukemia , antibody , biology , receptor , biochemistry , gene
Tumor necrosis factor alpha (TNFα) is a pleiotropic cytokine that is constitutively produced by leukemic cells in B Chronic Lymphocytic Leukemia (B‐CLL). It has been shown to have autocrine and paracrine functions in normal B cells and in B lymphoproliferative diseases. This study was conducted to determine the effect of TNFα (in vitro) on CD20 expression on cells from patients with B‐CLL. Currently, anti‐CD20 monoclonal antibody therapy is becoming a second line treatment in the management of B cell disorders like low‐grade non‐Hodgkin's lymphoma (NHL) and B‐CLL. Our results demonstrate amply that very low doses of TNFα (0.0125 ng/ml) can be used to significantly increase CD20 expression on cells from patients of B‐CLL as evidenced by increases in both percentage positivity and mean fluorescence intensity. The upregulation is evident as early as 24 hours and is maintained for up to 72 hours. We propose that the upregulation is a direct result of in vitro differentiation stimulated by TNFα. The results presented can be exploited in the designing of priming protocols prior to antibody therapy and this is discussed. Microsc. Res. Tech. 50:251–257, 2000. © 2000 Wiley‐Liss, Inc.