ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02781.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02782.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02783.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

High‐density lipoprotein (HDL) apolipoprotein was separated from hamster serum by cholesteryl hemisuccinate atlinity chromatography (CHAC) in comparison with the density‐gradient ultracentrifugation (DGUC), The apolipoprotein recovery from scrum by CHAC was 70% and by DGUC 80%, This disadvantage is compensated for by the ease of purification by CHAC, a method particularly suited for the processing of large amounts of serum.From the acute‐phase HDL CHAC fraction, apo SAA was isolated by gel filtration. Using isoelectrofocusing, two‐dimensional gel electrophoresis, und titration curve, four isotypes of hamster apo SAA were identified and characterized In the acute‐phase serum, one of the isotypes was predominant (apo SAA1), In serum of amyloidotic animals, the relative contribution of apo SAAlwas considerably lower, suggesting selective removal of the latter during amyloidogencsis and possibly its deposition in hamster AA amyloid. Furthermore, the affinity chromatography method was modified with gradient elution of affinity‐bound material. By this method HDL apolipoprotein was separated into three subclasses. Apo SAA was shown to associate with two different subclasses. In acute‐phase serum most of the apo SAA1was found in the subclass with the lowest affinity for the cholesteryl beads, whereas thc latter was depressed in amyloidotic serum, suggesting that the amyloidogenicity ofa particular apo SAA isotype is determined by its cholesteryl‐bin

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02784.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

ZnCl2exerted a dose‐dependent inhibition of citrate‐phosphate dextrose (CPD) plasma‐induced release of125I‐labelled BSA‐anti‐BSA immune complexes (IC) bound to complement receptor lype I (CRl. CD35) in human whole blood. Maximal inhibition was observed at 10mM of ZnCl2.Furthermore, the release of IC bound to erythrocyte (E)‐CRI by purified factor I. factor Ideficient serum plus purified factor I. or normal human. Serum was reduced by approximately 90%, 64%, and 52%, respectively, in the presence of 10 mM ZnCl2.The effect of ZnCl2on factor 1‐mediated degradation of cell‐bound C3b/C4b was also investigated employing CPD blood or E from a factor I‐deficient donor. These cells expressed covalently bound C3b and C4b as demonstrated by a simple agglutination technique. Upon incubation of CPD whole blood with purified factor I. or of E wilh purified factor I or normal CPD plasma, the C‐fragments were cleaved and the cells were no longer agglutinated by antibodies to C3c and C4c. The presence of ZnCl2prevented Ihis factor 1‐mediaied degradation of C3b and C4b, as evidenced by the unaffected agglutination of the cells by the antibodies.We conclude that ZnCl2inhibited factor I aclivity since: (1) release of complementpreopsonized IC from E‐CR 1 by purified factor I was markedly inhibited (90%) in the presence of ZnCl2, (2) preincubation of the cells with ZnCl2caused only a moderate inhibition (32 38%) of the IC release, and (3) degradation by purified factor I of covalently cell‐bound C3 band C4b was abrogated in

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02785.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Restriction fragment length polymorphism using an HLA‐DQ β‐chain genomic probe showed that 63 children with insulin‐dependent (type 1) diabetes mellitus (IDDM) were all (100%) positive for the BamH1 fragments 12 kb and/or 4 kb compared to 98% (62/63) for HLA‐DR3 and/or 4 and 75% (47/63) for HLA‐B8 and/or 15. The 36 (56%) DR3‐positive children were all 4‐kb‐positive; however, a total of 44 (70%) children were 4‐kb‐positive (P<0.02). The 55 (87%) DR4‐positive children were all 12‐kb‐positive, but a total of 56 (89%) were 12‐kb‐positive (NS), The heterozygosity at the HLA region increased from 11/63 (18%) for HLA‐B8/15 to 29/63 (46%) for HLA‐DR3/4 (P<0,0004) and to 37/63 (59%) for the HLA‐DQ 4 kb/12 kb fragments (P<0.02). The test of an equal probability ofa positive result under the adjacent pair of tests indicates that the increased risk of developing IDDM in association with HLA‐DQ is to a great extent due to heterozygosity at this locus. There were no differences between the 4 kb/12 kb and the DR3/4‐positive IDDM children with respect to fasting or meal‐stimulated C peptide, insulin requirement, or levels of insulin antibodies formed during the first 12 months of insulin therapy. Our results support the hypothesis that HLA‐DQ is closely associated with an increased risk of childhood IDDM, and when typed for at this locus parameters of the clinical course were homogeneous, suggesting that factors other than HLA‐DQ may determine previously observed differences between IDDM

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02786.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Taking advantage ofthe polymerase chain reaction we have studied the usage of variable delta‐(Vδ)) region genes in freshly isolated synovial fluid T cells from patients with rheumatoid synovitis. Amplified mRNA from one patient with rheumatoid arthritis (RA) was cloned into an Smaleleaved pUC19 vector and colonies were screened with probes for three of the known human variable δ‐gene families (Vδ1. Vδ2. Vδ3). Of 10 clones, seven used Vδl. two Vδ2 and one Vδ3. This pattern of distribution is different from that of normal peripheral blood, where approximately 60% of Tγδ) cells are reported to use the Vδ2 gene. Furthermore, Northern blot hybridization analyses of mononuclear cells from two additional synovial fluids derived from another patient with RA and one with juvenile rheumatoid arthritis (JRA) also showed significant hybridization only with Vδ I. In summary, these preliminary results suggest a usage of Vδ gene families in Tγδ lymphocytes in synovial fluid of rheumatoid patients different to that found in norma

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02787.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

We have activated B cells with membrane‐incorporated monoclonal antibodies against the hapten trinitrophenyl (TNP) using various concentrations of the polyclonal activator lipopolysaccharide (LPS) haptenated with TNP, We found that anti‐TNP‐decorated B cells were polyclonally activated by 1000‐fold lower concentrations of TNP LPS than untreated B cells or B cells decorated with antibodies of other specificities. In order to test whether the passively incorporated anti‐TNP monoclonals could mediate activation signals or only served to focus the polyclonal activator TNP‐LPS to the B cells, we compared the response of anti‐TNP‐decorated B cells from normal C3H/He mice and from the LPS‐unresponsive strain C3H/HeJ. We found that B cells from C3H/HeJ mice could not be activated to polyclonal antibody synthesis, in contrast to B cells from the LPS‐responsive strain C3H/He. Thus, contrary to what was previously suggested [9], the incorporated anti‐TNP antibodies could not mediate activation signals, but only served to passively bind and concentrate TNP‐LPS to the membrane of the B cells, thereby increasing the concentration of the polyclonal B‐cell act

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02788.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

In this study we investigated the binding or three different monoclonal antibodies (MoAb), TII 19‐4‐7,4EL1C7, and B1.19.2, which are clustered in CD26 to the ectoenzyme dipeptidyl peptidase IV (DPP IV) and to T lymphocytes. We found that all three MoAb bind to both unstimulated and mitogen‐stimulated T lymphocytes. Further results indicated an inconsistency within the CD26‐clusteredMoAb: TII 19‐4‐7 and 4EL1C7, but not Bl.19.2, recognized DPP IV on the surface of T lymphocytes and immobilized on solid‐phase ELISA or Western blot. There was compelition of binding to DPP IV between TII 19‐4‐7 and 4ELIC7. From these results we conclude that CD26 antigen is represented by the ectoenzyme DPP IV. TII 19‐4‐7 and 4ELIC7 recognize the same or partly identical epitopes on DPP IV, whereas B1.19.2 recognizes a different antigen. TI I 19‐4‐7 and 4ELlC7, but not B1.19.2, sh

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02789.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY

摘要:

Our aim was to investigate why serum IgM is poorly transferred into secretions in normal subjects. Indeed, the low IgM level in secretions contrasts with the eapacity of monoclonal IgM to bind to secretory component (SC), but it is not well established to what extent normal serum IgM can do so.The mean SC affinity was studied with a polyclonal IgM preparation from 250 normal subjects and with a representative pool of 100 different monoclonal IgM. The SC‐binding percentages varied as a function of the IgM/SC molar ratio according to a common hyperbolic curve, with similar association constants:Ka= 4.19 ± 2.61 × 107M‐1(polyclonal pool) andKa= 5.8 0 ± 2.73 × 107(monoclonal pool). It thus appears that the large difference in IgM concentrations between blood and secretions cannot be due to an SC‐binding defect of serum IgM, but is probably explained by its low diffusion from blood to the extravascular compartment, co

ISSN:0300-9475    

DOI:10.1111/j.1365-3083.1990.tb02790.x

出版商:Blackwell Publishing Ltd    

年代:1990

数据来源: WILEY