Immune Abnormalities

Early in the disease, the absolute number of T cells may be increased with inversion of the T-helper to T-suppressor cell ratio.41-43 The CD4/CD8 ratio may continue to drop with disease progression or after successful therapy with nucleoside analogues. Additionally, a decreased proportion of cells express the CD3 antigen. The T cells may respond normally to mitogens, such as phytohemagglutinin, in vitro and produce interleukin-2 and gamma-interferon,44 but their reactivity to allogeneic and autologous B cells is impaired.45,46 Functional studies of the T cells have sometimes shown decreased T-helper functions.41,45,47 Spontaneous and antibody-dependent cytotoxicity are decreased, which suggests an abnormality in the large granular lymphocyte population, including natural killer (NK) cells.48 The etiology of these disturbances is not clear. One possibility is that T- and NK-cell functions may be suppressed by factors produced by CLL B cells.49 The pathogenesis of hypogammaglobulinemia in CLL is poorly understood. However, impaired B-cell function, as well as regulatory abnormalities of T cells, including the reversal of normal helper/suppressor cell ratios, may play a role. Furthermore, CLL-derived NK cells have been shown to suppress immunoglobulin secretion by normal B cells in vitro.50

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