DEFICIENCY OF COMPLEMENT DECAY-ACCELERATING FACTOR (DAF, CD55) IN NON-HODGKINS-LYMPHOMA

被引:12
作者
FUKUDA, H
SEYA, T
HARA, T
MATSUMOTO, M
KINOSHITA, T
MASAOKA, T
机构
[1] CTR ADULT DIS,DEPT IMMUNOL,HIGASHINARI KU,OSAKA 537,JAPAN
[2] CTR ADULT DIS,DEPT HEMATOL,OSAKA 537,JAPAN
[3] OSAKA UNIV,MICROBIAL DIS RES INST,SUITA,OSAKA 565,JAPAN
关键词
DEPOSITION OF COMPLEMENT C3; DECAY-ACCELERATING FACTOR (DAF; CD55); MEMBRANE COFACTOR PROTEIN (MCP; CD46); NON-HODGKINS LYMPHOMA;
D O I
10.1016/0165-2478(91)90171-6
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We have assessed levels of surface-expressed complement regulatory proteins, decay-accelerating factor (DAF) and membrane cofactor protein (MCP) on cells from patients with hematological malignancies. Neither malignant cells nor unaffected nucleated blood cells from the patients lacked MCP. On the other hand, complete deficiency of DAF was found in 2/10 of non-Hodgkin's lymphoma (NHL), while none of the 38 patients with acute nonlymphocytic leukemia (ANLL) (14 cases), chronic myelogenous leukemia (CML) (6 cases), acute lymphocytic leukemia (ALL) (12 cases) and chronic lymphocytic leukemia (CLL) (6 cases) lacked DAF. The two patients with DAF-negative NHL had no history of paroxysmal nocturnal hemoglobinuria (PNH), and their peripheral blood cells were DAF-positive. One DAF-negative NHL exhibited T cell markers and the other those of B cell. In both cases, treatment of the DAF-negative lymphoma cells with antibody against MCP (M177) followed by Mg2+-EGTA-serum resulted in efficient deposition of homologous C3. These results infer that some NHL specifically lack DAF and, through treatment with M177, are targeted by homologous C3.
引用
收藏
页码:205 / 210
页数:6
相关论文
共 30 条
[1]   SEPARATION OF SELF FROM NON-SELF IN THE COMPLEMENT-SYSTEM [J].
ATKINSON, JP ;
FARRIES, T .
IMMUNOLOGY TODAY, 1987, 8 (7-8) :212-215
[2]  
BESSIS M, 1976, BLOOD SMEARS REINTER
[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]   CD59, AN LY-6-LIKE PROTEIN EXPRESSED IN HUMAN LYMPHOID-CELLS, REGULATES THE ACTION OF THE COMPLEMENT MEMBRANE ATTACK COMPLEX ON HOMOLOGOUS CELLS [J].
DAVIES, A ;
SIMMONS, DL ;
HALE, G ;
HARRISON, RA ;
TIGHE, H ;
LACHMANN, PJ ;
WALDMANN, H .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 170 (03) :637-654
[5]   REGULATION OF THE AMPLIFICATION C-3 CONVERTASE OF HUMAN-COMPLEMENT BY AN INHIBITORY PROTEIN ISOLATED FROM HUMAN-ERYTHROCYTE MEMBRANE [J].
FEARON, DT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1979, 76 (11) :5867-5871
[6]   THE MECHANISM OF ACTION OF DECAY-ACCELERATING FACTOR (DAF) DAF INHIBITS THE ASSEMBLY OF C-3 CONVERTASES BY DISSOCIATING C2A AND BB [J].
FUJITA, T ;
INOUE, T ;
OGAWA, K ;
IIDA, K ;
TAMURA, N .
JOURNAL OF EXPERIMENTAL MEDICINE, 1987, 166 (05) :1221-1228
[7]   PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA TYPE-III - LACK OF AN ERYTHROCYTE-MEMBRANE PROTEIN RESTRICTING THE LYSIS BY C5B-9 [J].
HANSCH, GM ;
SCHONERMARK, S ;
ROELCKE, D .
JOURNAL OF CLINICAL INVESTIGATION, 1987, 80 (01) :7-12
[8]   ISOLATION AND CHARACTERIZATION OF A MEMBRANE-PROTEIN FROM NORMAL HUMAN-ERYTHROCYTES THAT INHIBITS REACTIVE LYSIS OF THE ERYTHROCYTES OF PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA [J].
HOLGUIN, MH ;
FREDRICK, LR ;
BERNSHAW, NJ ;
WILCOX, LA ;
PARKER, CJ .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 84 (01) :7-17
[9]   MEMBRANE-BOUND C4B INTERACTS ENDOGENOUSLY WITH COMPLEMENT RECEPTOR CR-1 OF HUMAN RED-CELLS [J].
KINOSHITA, T ;
MEDOF, ME ;
HONG, K ;
NUSSENZWEIG, V .
JOURNAL OF EXPERIMENTAL MEDICINE, 1986, 164 (05) :1377-1388
[10]   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