We have now discovered several patients with hypocomplementemia associated with chronic lymphocytic leukemia (CLL) and circulating immune complexes in their sera. In addition, in a few patients anti-lymphocyte antibodies were found by C-dependent cytotoxicity and indirect immunofluorescence (Day et al., Clin. Exp. Immunol., 1976). We have postulated that one of the mechanism(s) by which C is depleted is the direct interaction of the anti-lymphocyte antibody and the circulating CLL lymphocytes. This study examined the presence of C1̄ on lymphocytes obtained from normal healthy individuals and from CLL patients with hypo- or hyper-complementemia, using the C1 transfer and C4 consumption tests. Studies of lymphocytes from normal subjects revealed that: 1) In 10 different normal donors 6.0 to 23.8 molecules of C1 per lymphocyte were detected by the C1 transfer test; 2) Lymphocytes could inactivate C4 after incubation with purified C4; 3) C1 could not be detected on erythrocytes, platelets, or monocytes; 4) EDTA treatment of lymphocytes removed C1 from their surfaces and, hence, abolished their ability to consume C4.

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