B-cell chronic lymphocytic leukemia cells express a surface membrane phenotype of activated, antigen-experienced B lymphocytes: Presented in part at the 42nd …

RN Damle, F Ghiotto, A Valetto… - Blood, The Journal …, 2002 - ashpublications.org
RN Damle, F Ghiotto, A Valetto, E Albesiano, F Fais, XJ Yan, CP Sison, SL Allen, J Kolitz…
Blood, The Journal of the American Society of Hematology, 2002ashpublications.org
B-cell chronic lymphocytic leukemia (B-CLL) is considered an accumulative disease of
antigen-naive CD5+ B lymphocytes that circulate in the resting state. However, to evaluate
the possibility that B-CLL cells resemble antigen-experienced and activated B cells, we
analyzed the expression of markers of cellular activation and differentiation on CD5+ CD19+
cells from B-CLL patients and from age-matched healthy donors. The leukemic cells from all
B-CLL patients, including those that lack significant numbers of V gene mutations, bear the …
B-cell chronic lymphocytic leukemia (B-CLL) is considered an accumulative disease of antigen-naive CD5+ B lymphocytes that circulate in the resting state. However, to evaluate the possibility that B-CLL cells resemble antigen-experienced and activated B cells, we analyzed the expression of markers of cellular activation and differentiation on CD5+CD19+ cells from B-CLL patients and from age-matched healthy donors. The leukemic cells from all B-CLL patients, including those that lack significant numbers of V gene mutations, bear the phenotype of activated B cells based on the overexpression of the activation markers CD23, CD25, CD69, and CD71 and the underexpression of CD22, Fcγ receptor IIb, CD79b, and immunoglobulin D that are down-regulated by cell triggering and activation. Furthermore, these leukemic cells resemble antigen-experienced lymphocytes in the underexpression of molecules that are down-regulated by cell triggering and in the uniform expression of CD27, an identifier of memory B cells. A comparison of the phenotypes of B-CLL patients with and without immunoglobulin V gene mutations suggests that the 2 subgroups differ both in specific marker expression (CD69, CD71, CD62 L, CD40, CD39, and HLA-DR) and in the time since antigenic stimulation, based on the reciprocal relationship of CD69 and CD71 expression. These findings imply that the leukemic cells from all B-CLL cases (irrespective of V gene mutations) exhibit features of activated and of antigen-experienced B lymphocytes and that the B-CLL cells that differ in immunoglobulin V genotype may have different antigen-encounter histories.
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