Capping of peripheral blood lymphocyte C3 receptors in chronic lymphocytic leukemia: Relationship to chemotherapy

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Abstract
The data show that in chronic lymphocytic leukemia (CLL) there are elevated numbers of peripheral blood lymphocytes (PBL) capable of rosette formation (complement‐rosetting lymphocytes, CRL) with bacteria (B)‐antibody‐(A)‐complement (C) (BAC) complexes. In most of the CLL patients studied, large percentages of CRL were impaired in their ability to undergo BAC‐C3R cap formation compared to normal donors. The degree of impairment varied from one patient to the next. A consideration of clinical information suggested that the variation was related to the clinical response of patients to chemotherapy. Four categories of CLL patients could be identified on the basis of clinical data: (1) patients who had never received therapy for CLL; (2) those whose clinical history indicated a failure to respond to ongoing chemotherapy; (3) patients who had received successful prior chemotherapy and who were asymptomatic or stable and were receiving no therapy at the time of study; and (4) those who were undergoing therapy at the time of study and who subsequently became stable or asymptomatic and were removed from therapy. The first two categories of patients failed to show significant BAC‐C3R capping, whereas the last two were able to form C3R caps on significant percentages of CRL No direct relationship could be discerned between C3R capping and currently accepted classifications or stages (Rai) of CLL. These results suggest that monitoring the percentages of BAC‐C3R cap‐forming CRL may be useful in determining the success of chemotherapy of CLL patients. The microtubule‐disrupting agent colchicine enhanced BAC‐C3R capping in all CLL patients to normal levels, whereas the microfilament‐disrupting agent cytochalasin B (CB) had no effect on CLL PBL C3R capping. CB totally abolished C3R capping of CRL from normal donors. These results suggest that abnormalities exist in both cytoskeletal and contractile systems of CRL from CLL peripheral blood.