LAUSR

1 (PD-1) on total CD4, total CD8 and T helper cells, and cytotoxic T lymphocyte-associated antigen-4 on total CD4 (P=0.010) and regulatory T cells (P<0.05) reduced after treatment (P<0.05). There were significant differences in expression intensity of CD19 (P<0.01), C-X-C chemokine receptor type 5 (CXCR5) (P<0.01) and CD49d (P<0.05) on B cells before and after treatment. Down-regulation of PD-1 on T cells and CXCR5 and CD19 on B cells were observed in nearly all patients after zanubrutinib treatment. The number of B cells and programmed death-ligand 1 expression down-regulated, especially in the young, CLL, normal spleen, normal β2-macroglobulin (β2-MG), abnormal lactate dehydrogenase (LDH) and normal tumor protein 53 subgroups, while CD49d expression tended to decrease in the male, old, CLL, splenomegaly, abnormal β2-MG and abnormal LDH subgroups after zanubrutinib treatment. Conclusions: These findings suggest that zanubrutinib can regulate immunity primarily by improving T cell exhaustion, inhibiting suppressor cells and disrupting CLL cells migration through down-regulation of adhesion/homing receptors. Furthermore, favorable changes in cell number and immunophenotype were preferably observed in patients without adverse prognostic factors.