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A Comparative Study of C1̄ on Normal Lymphocytes and on Lymphocytes from Patients with Chronic Lymphocytic Leukemia (CLL)
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Abstract
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. 5) EDTA-treated lymphocytes could bind exogenous C1; 6) Pretreatment with C1̄-INA decreased the number of C1 molecules detected on lymphocytes and inhibited the ability of lymphocytes to consume C4, and 7) Lymphocytes could inactivate C2 when incubated with C2 in the presence of C4. These findings indicated that washed lymphocytes behave like EAC1. A comparative study between EDTA-treated lymphocytes and EA revealed that 1) the efficiency of C1 binding by lymphocytes was much less than that by EA and 2) the consumption of C4 by lymphocyte-bound C1 was more effective than that by C1 bound to EA.
Title: A Comparative Study of C1̄ on Normal Lymphocytes and on Lymphocytes from Patients with Chronic Lymphocytic Leukemia (CLL)
Description:
Abstract
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.
5) EDTA-treated lymphocytes could bind exogenous C1; 6) Pretreatment with C1̄-INA decreased the number of C1 molecules detected on lymphocytes and inhibited the ability of lymphocytes to consume C4, and 7) Lymphocytes could inactivate C2 when incubated with C2 in the presence of C4.
These findings indicated that washed lymphocytes behave like EAC1.
A comparative study between EDTA-treated lymphocytes and EA revealed that 1) the efficiency of C1 binding by lymphocytes was much less than that by EA and 2) the consumption of C4 by lymphocyte-bound C1 was more effective than that by C1 bound to EA.
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