Reduced phagocytic activity of polymorphonuclear leukocytes in α(1,3) fucosyltransferase VII-deficient mice

被引:3
作者
Bartunkova, J [1 ]
Maly, P [1 ]
Smetana, K [1 ]
Sedivá, A [1 ]
Klubal, R [1 ]
Mayerová, D [1 ]
Sedlácek, A [1 ]
Splíchalová, V [1 ]
机构
[1] Charles Univ Prague, Fac Med 2, Inst Immunol, Prague 15006 5, Czech Republic
关键词
alpha(1,3)fucosyltransferase VII; selectin ligand; adhesion molecules; gene knock-out; phagocytosis;
D O I
10.1034/j.1600-0463.2000.d01-76.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Deficiencies in adhesion molecules or their counter-receptors in humans may have severe consequences as exemplified by leukocyte adhesion deficiency (LAD) I or II syndromes. Because such diseases occur with great rarity, animal models are valuable for studying the role of particular adhesion molecules and their natural ligands in immunity. We studied selected immune parameters and general health in mice with a defect in the sialyl-Lewis X antigen (selectin ligand) caused by disruption of the gene encoding alpha(1,3)fucosyltransferase VII (Fuc-TVII). Leukocytes from Fuc-TVII -/- and control mice were tested for adherence to cellophane membranes or polymer particles in vivo and phagocytic activity in vitro. While no difference in adherence was found, the number of neutrophil granulocytes in exudate induced by intraperitoneal injection of polymer beads was reduced in knock-out mice. Moreover, the phagocytic activity in Fuc-TVII -/- mice was significantly reduced. These animals have splenomegaly due to increased hematopoiesis and reduced weight but do not exhibit clinical signs of immunodeficiency. In conclusion, the lack of Fuc-TVII activity leads to several morphological and functional abnormalities without an impact on survival rate.
引用
收藏
页码:409 / 416
页数:8
相关论文
共 27 条
[1]   LEUKOCYTE ADHESION DEFICIENCY - AN INHERITED DEFECT IN THE MAC-1, LFA-1, AND P150,95 GLYCOPROTEINS [J].
ANDERSON, DC ;
SPRINGER, TA .
ANNUAL REVIEW OF MEDICINE, 1987, 38 :175-194
[2]   LYMPHOCYTE HOMING AND LEUKOCYTE ROLLING AND MIGRATION ARE IMPAIRED IN L-SELECTIN-DEFICIENT MICE [J].
ARBONES, ML ;
ORD, DC ;
LEY, K ;
RATECH, H ;
MAYNARDCURRY, C ;
OTTEN, G ;
CAPON, DJ ;
TEDDER, TF .
IMMUNITY, 1994, 1 (04) :247-260
[3]   Autoimmunity to polymorphonuclears: Functional consequences of the binding of antibodies to membrane and cytoplasmic target antigens of polymorphonuclear leukocytes [J].
Bartunkova, J ;
Araujo, A ;
Hrusak, O ;
Sediva, A .
JOURNAL OF CLINICAL IMMUNOLOGY, 1997, 17 (06) :455-461
[4]   Lymphocyte homing and homeostasis [J].
Butcher, EC ;
Picker, LJ .
SCIENCE, 1996, 272 (5258) :60-66
[5]   RECURRENT SEVERE INFECTIONS CAUSED BY A NOVEL LEUKOCYTE ADHESION DEFICIENCY [J].
ETZIONI, A ;
FRYDMAN, M ;
POLLACK, S ;
AVIDOR, I ;
PHILLIPS, ML ;
PAULSON, JC ;
GERSHONIBARUCH, R .
NEW ENGLAND JOURNAL OF MEDICINE, 1992, 327 (25) :1789-1792
[6]   Adhesion defects - from mice to humans [J].
Etzioni, A .
MOLECULAR IMMUNOLOGY, 1998, 35 (11-12) :691-691
[7]   MOLECULAR-CLONING, EXPRESSION, CHROMOSOMAL ASSIGNMENT, AND TISSUE-SPECIFIC EXPRESSION OF A MURINE ALPHA-(1,3)-FUCOSYL-TRANSFERASE LOCUS CORRESPONDING TO THE HUMAN ELAM-1 LIGAND FUCOSYL-TRANSFERASE [J].
GERSTEN, KM ;
NATSUKA, S ;
TRINCHERA, M ;
PETRYNIAK, B ;
KELLY, RJ ;
HIRAIWA, N ;
JENKINS, NA ;
GILBERT, DJ ;
COPELAND, NG ;
LOWE, JB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (42) :25047-25056
[8]   HIGH ENDOTHELIAL VENULES (HEVS) - SPECIALIZED ENDOTHELIUM FOR LYMPHOCYTE MIGRATION [J].
GIRARD, JP ;
SPRINGER, TA .
IMMUNOLOGY TODAY, 1995, 16 (09) :449-457
[9]   Leukocyte Adhesion Deficiency Type II is a generalized defect of de novo GDP-fucose biosynthesis - Endothelial cell fucosylation is not required for neutrophil rolling on human nonlymphoid endothelium [J].
Karsan, A ;
Cornejo, CJ ;
Winn, RK ;
Schwartz, BR ;
Way, W ;
Lannir, N ;
Gershoni-Baruch, R ;
Etzioni, A ;
Ochs, HD ;
Harlan, JM .
JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (11) :2438-2445
[10]  
Knibbs RN, 1998, J IMMUNOL, V161, P6305