CLL patients have an increased risk of developing bacterial infections (47-49). Different reasons have been offered for this infection predisposition, especially the presence of hypo-gammaglobulinemia. Rozman et al. (50) investigated the prognostic significance of gamma-globulin and immunoglobulin levels in chronic lymphocytic leukemia. The survival probability of patients with initial levels of gammaglobulin of less than 700 mg/dL was significantly lower than that of patients with initial levels of 700 mg/dL or more. On the other hand, the worse prognosis observed in patients with low Ig levels did not seem to be necessarily correlated with an excess of severe infections in these patients. In line with this finding, other investigators were unable to demonstrate a relationship between hypogammaglobulinemia and reduced overall survival (51-53).
T-cell immunodeficiency has also been implicated in the increased number of infections and was correlated with prognosis (54-56). Totterman et al. (55) showed that CLL patients had an increase in the absolute number of phenotypically activated, HLA-DR+ CD4+ and CD8+ cells and T suppressor/effector (CD11b+/CD8+) cells, but in more advanced clinical stages a reduced proportion of T-suppressor/effector (CD11b+) cells was shown.
A number of soluble molecules may have an impact on the immune system. Thus, leukemic B-cells, through the elaboration of suppressive cytokines such as transforming growth factor-P (TGF-P) and release of soluble CD27, downregulate the expression of CD40 ligands (CD154), originally expressed by CD4-positive T-cells after immune activation (57-60). Such down-regulation has been considered responsible, at least in part, for the immune deficiency that is acquired in CLL (61). Finally, immunodeficiency has been correlated with the presence of autoimmune phenomena, probably by accumulating anergic self-reactive CD5+ B-cells (62,63).
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