LEVELS OF COMPLEMENT REGULATORY PROTEINS, CD35 (CR-1), CD46 (MCP) AND CD55 (DAF) IN HUMAN HEMATOLOGICAL MALIGNANCIES

被引:78
作者
HARA, T
KOJIMA, A
FUKUDA, H
MASAOKA, T
FUKUMORI, Y
MATSUMOTO, M
SEYA, T
机构
[1] CTR ADULT DIS, DEPT IMMUNOL, HIGASHINARI KU, OSAKA 537, JAPAN
[2] CTR ADULT DIS, DEPT HAEMATOL, HIGASHINARI KU, OSAKA 537, JAPAN
[3] OSAKA RED CROSS BLOOD CTR, HIGASHINARI KU, OSAKA 537, JAPAN
关键词
D O I
10.1111/j.1365-2141.1992.tb06431.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Levels of the membrane complement regulatory proteins, C3b/C4b receptor (CR1, CD35), membrane cofactor protein (MCP, CD46), and decay-accelerating factor (DAF, CD55), expressed on cells from patients with haematological malignancies and normal subjects were assessed by flowcytometry using the respective monoclonal antibodies (mAbs). All myeloid and most lymphoid leukaemia samples tested were CR1-negative: two of the 42 leukaemia samples expressed minute amounts of CR1. Lack of CR1 in leukaemia cells was confirmed with two mAbs raised against CR1, 31R, and 243R, which recognized different epitopes and induced different degrees of CR1-mediated fluorescent shift on flowcytometry in granulocytes and erythrocytes. MCP was increased in most chronic myelogenous leukaemia (CML) and chronic lymphocytic leukaemia (CLL), and was also increased in majority of acute nonlymphocytic leukaemia (ANLL), acute lymphocytic leukaemia (ALL) and non-Hodgkin's lymphoma (NHL). Levels of DAF were also high in CML and CLL, and were variable in other types of leukaemia: some were DAF-negative while others expressed extremely high levels of DAF. In CML patients, the high level of MCP and the lack of CR1 were normalized after medical treatment. These results are in agreement with the data obtained with human leukaemia cell lines, and support the hypothesis that CR1 is essentially a differentiated cell antigen and that a high level of MCP reflects some malignant transformation or an immature stage in blood cells.
引用
收藏
页码:368 / 373
页数:6
相关论文
共 24 条
[1]   BIOSYNTHESIS OF THE HUMAN C3B/C4B RECEPTOR DURING DIFFERENTIATION OF THE HL-60 CELL-LINE - IDENTIFICATION AND CHARACTERIZATION OF A PRECURSOR MOLECULE [J].
ATKINSON, JP ;
JONES, EA .
JOURNAL OF CLINICAL INVESTIGATION, 1984, 74 (05) :1649-1657
[2]  
BARTOW T J, 1989, Complement and Inflammation, V6, P312
[3]   DECAY-ACCELERATING FACTOR PROTECTS HUMAN-TUMOR CELLS FROM COMPLEMENT-MEDIATED CYTO-TOXICITY INVITRO [J].
CHEUNG, NKV ;
WALTER, EI ;
SMITHMENSAH, WH ;
RATNOFF, WD ;
TYKOCINSKI, ML ;
MEDOF, ME .
JOURNAL OF CLINICAL INVESTIGATION, 1988, 81 (04) :1122-1128
[4]   THE ROLE OF C3 IN THE IMMUNE-RESPONSE [J].
ERDEI, A ;
FUST, G ;
GERGELY, J .
IMMUNOLOGY TODAY, 1991, 12 (09) :332-337
[5]  
FEARON DT, 1983, SPRINGER SEMIN IMMUN, V6, P159
[6]   DEFICIENCY OF COMPLEMENT DECAY-ACCELERATING FACTOR (DAF, CD55) IN NON-HODGKINS-LYMPHOMA [J].
FUKUDA, H ;
SEYA, T ;
HARA, T ;
MATSUMOTO, M ;
KINOSHITA, T ;
MASAOKA, T .
IMMUNOLOGY LETTERS, 1991, 29 (03) :205-210
[7]   HUMAN-COMPLEMENT C3B/C4B RECEPTOR (CR-1) MESSENGER-RNA POLYMORPHISM THAT CORRELATES WITH THE CR-1 ALLELIC MOLECULAR-WEIGHT POLYMORPHISM [J].
HOLERS, VM ;
CHAPLIN, DD ;
LEYKAM, JF ;
GRUNER, BA ;
KUMAR, V ;
ATKINSON, JP .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (08) :2459-2463
[8]   THE REGULATORS OF COMPLEMENT ACTIVATION (RCA) GENE-CLUSTER [J].
HOURCADE, D ;
HOLERS, VM ;
ATKINSON, JP .
ADVANCES IN IMMUNOLOGY, 1989, 45 :381-416
[9]   DISTRIBUTION OF DECAY-ACCELERATING FACTOR IN THE PERIPHERAL-BLOOD OF NORMAL INDIVIDUALS AND PATIENTS WITH PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA [J].
KINOSHITA, T ;
MEDOF, ME ;
SILBER, R ;
NUSSENZWEIG, V .
JOURNAL OF EXPERIMENTAL MEDICINE, 1985, 162 (01) :75-92
[10]   CYTOLYSIS OF NUCLEATED CELLS BY COMPLEMENT - CELL-DEATH DISPLAYS MULTI-HIT CHARACTERISTICS [J].
KOSKI, CL ;
RAMM, LE ;
HAMMER, CH ;
MAYER, MM ;
SHIN, ML .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1983, 80 (12) :3816-3820