Table 3a. . Treatment with rituximab-cyclophosphamide–doxorubicin–vincristine–prednisone induces a ‘Kamikaze effect’ with a reduction of natural killer cells.
| All patients | NK pre-R-CHOP | NK after-R-CHOP | NK (1 Ritux) | NK (3 Ritux) | NK (6 Ritux) |
|---|---|---|---|---|---|
| 52 | 73 | 176 | 217 | 215 | |
| 262 | 27 | 188 | 176 | 132 | |
| 163 | 65 | 103 | 85 | 230 | |
| 256 | 66 | 95 | 132 | 195 | |
| 135 | 73 | 52 | 74 | 117 | |
| 108 | 95 | 180 | 329 | 230 | |
| 854 | 124 | 232 | 184 | 117 | |
| 230 | 162 | 333 | 498 | ||
| 177 | 341 | 233 | 228 | ||
| 291 | 423 | 369 | |||
| Xme | 163 | 84 | 176 | 201 | 222 |
| (Xmin–Xmax) | (52–854) | (27–291) | (52–341) | (74–423) | (117–498) |
Bold details are only to differentiate patients that receive intravenous rituximab from the patients with subcutaneous rituximab.
Effector cells (NK cells) are slightly below normal reference values (87 NK cells/ml), improved however, during maintenance with rituximab effector cells (NK cells). Rituximab maintenance therapy causes the encounter of effector cells (NK cells) with monoclonal antibody, but without target cells (leukemia or lymphoma blood cells), in blood compartment. This may be a model of the distribution of NK cells in the presence of anti-CD20 antibodies without target cells and may help to explain the phenomenon in which some patients with deep responses to obinutuzumab recover NK cell counts when nontumoral cells in blood or secondary lymphoid organs may be located.
NK: Natural killer; R-CHOP: Rituximab–cyclophosphamide–doxorubicin–vincristine–prednisone; Xmax: Maximal value; Xme: Median X value; Xmin: Minimun value.