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Pathogenesis of Impaired Cellular Immune Function in CLL

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Part of the book series: Contemporary Hematology ((CH))

Abstract

B-cell chronic lymphocytic leukemia (B-CLL) is defined as a monoclonal B-cell malignancy with a characteristic cell surface phenotype including expression of both CD19 and CD5 antigens (see Chapter 7). The clinical events characterizing the patients who eventually progress are most often linked to an accumulation of clonal CD5+ leukemic cells, particularly in the bone marrow, lymph nodes, and spleen. Although the hallmark of the leukemic CLL B-cell is its resistance to apoptosis, there is no significant insight into the exact biological reasons for that seminal biological event. It is probably true that critical genetic events are primary and lead to the B-cell resistance to apoptosis. However, we would hypothesize that the role of the microenvironment, including tissue-specific stroma, cytokine levels, vascular supply, and the host immune system, contribute to the augmentation and/or stabilize CLL B-cell apoptotic resistance. Thus, we have been interested in the study of both the qualitative and quantitative nature of the immune system in B-CLL.

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Johnston, P.B., Kay, N.E. (2004). Pathogenesis of Impaired Cellular Immune Function in CLL. In: Faguet, G.B. (eds) Chronic Lymphocytic Leukemia. Contemporary Hematology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-412-2_5

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  • DOI: https://doi.org/10.1007/978-1-59259-412-2_5

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-61737-355-8

  • Online ISBN: 978-1-59259-412-2

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