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PMID |
Sentence |
1 |
1569346
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The two isotypes of the fourth complement component are C4A and C4B.
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2 |
1569346
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C4B forms ester bonds more efficiently than C4A and so, in theory, is more likely than C4A to bind to polysaccharide capsules of encapsulated bacteria.
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3 |
1569346
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The two isotypes of the fourth complement component are C4A and C4B.
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4 |
1569346
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C4B forms ester bonds more efficiently than C4A and so, in theory, is more likely than C4A to bind to polysaccharide capsules of encapsulated bacteria.
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5 |
2943202
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Tests for HLA-A, B, C, and DR; for complement proteins C2, C4A, C4B, and BF; and for the erythrocyte enzyme glyoxalase I were done in 17 nonresponders and 3 hyporesponders.
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6 |
2943202
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At least one of two extended haplotypes (B44, DR7, FC31 or B8, DR3, SCO1) were detected in 6 of the 9 who did not respond to revaccination, compared with 2 of 11 who responded to a second course of vaccine.
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7 |
7483776
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The investigation pointed out that many of these subjects carry HLA haplotypes classically involved in autoimmune diseases: namely HLADR7; DQ2, DR4; DQ8 and DR3; DQ2.
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8 |
7483776
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The polymorphism of Bf, C4A and C4B complement serum components, recognized as important "immune-function-related genes", pointed out an increased frequency of the null allele C4AQ0 (34.3 vs 6.8% of the controls) stressing the role of C4A serum complement component in response to foreign peptide.
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9 |
7631146
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For example, the extended haplotypes HLA-A1, B8, BfS, C4AQO, C4B1, DR3, DQ2 and HLA-A1, B8, BfF, C4A6, C4B2, DR3, DQ2 were present in nine of 34 cases of non-responders but only in one of 119 case of responders (P < 0.000001).
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10 |
8035031
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Binding of human immunodeficiency virus type 1 to the C3b/C4b receptor CR1 (CD35) and red blood cells in the presence of envelope-specific antibodies and complement.
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11 |
8834646
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[Reactivity to hepatitis B vaccination (HBV) in patients with uremia: association with defined HLA antigen configuration and complement protein allotypes C4A, C4B and B factor (Bf)].
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12 |
8834646
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Genes, which are responsible for the effectivity of immune response are located on the chromosome 6 similarly as the genes of the class I and II of the major histocompatibility complex (MHC) together with the genes of some complement proteins (C4A, C4B, B factor/Bf/).
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13 |
8834646
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The study investigates the interdependence between HLA configuration as well as complement protein allotypes (C4A, C4B, Bf) with the reactivity to HBV vaccination of ESRD [end stage renal disease]-patients. 153 ESRD-patients (68 females, 85 males; mean duration of hemodialysis therapy 8.2 +/- 5.1 years) were studied.
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14 |
8834646
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HLA typing was performed by means of microlymphocytotoxicity assay, whereas complement allotypes were estimated by using high voltage gel electrophoresis with subsequent specific immunofixation with antibodies against C4A, C4B and Bf.
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15 |
8834646
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In about 40% of NR HLA-A1, -B8, -DR3, or -DQ2 antigens occurred as homozygotes.
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16 |
8834646
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[Reactivity to hepatitis B vaccination (HBV) in patients with uremia: association with defined HLA antigen configuration and complement protein allotypes C4A, C4B and B factor (Bf)].
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17 |
8834646
|
Genes, which are responsible for the effectivity of immune response are located on the chromosome 6 similarly as the genes of the class I and II of the major histocompatibility complex (MHC) together with the genes of some complement proteins (C4A, C4B, B factor/Bf/).
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18 |
8834646
|
The study investigates the interdependence between HLA configuration as well as complement protein allotypes (C4A, C4B, Bf) with the reactivity to HBV vaccination of ESRD [end stage renal disease]-patients. 153 ESRD-patients (68 females, 85 males; mean duration of hemodialysis therapy 8.2 +/- 5.1 years) were studied.
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19 |
8834646
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HLA typing was performed by means of microlymphocytotoxicity assay, whereas complement allotypes were estimated by using high voltage gel electrophoresis with subsequent specific immunofixation with antibodies against C4A, C4B and Bf.
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20 |
8834646
|
In about 40% of NR HLA-A1, -B8, -DR3, or -DQ2 antigens occurred as homozygotes.
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21 |
8834646
|
[Reactivity to hepatitis B vaccination (HBV) in patients with uremia: association with defined HLA antigen configuration and complement protein allotypes C4A, C4B and B factor (Bf)].
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22 |
8834646
|
Genes, which are responsible for the effectivity of immune response are located on the chromosome 6 similarly as the genes of the class I and II of the major histocompatibility complex (MHC) together with the genes of some complement proteins (C4A, C4B, B factor/Bf/).
|
23 |
8834646
|
The study investigates the interdependence between HLA configuration as well as complement protein allotypes (C4A, C4B, Bf) with the reactivity to HBV vaccination of ESRD [end stage renal disease]-patients. 153 ESRD-patients (68 females, 85 males; mean duration of hemodialysis therapy 8.2 +/- 5.1 years) were studied.
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24 |
8834646
|
HLA typing was performed by means of microlymphocytotoxicity assay, whereas complement allotypes were estimated by using high voltage gel electrophoresis with subsequent specific immunofixation with antibodies against C4A, C4B and Bf.
|
25 |
8834646
|
In about 40% of NR HLA-A1, -B8, -DR3, or -DQ2 antigens occurred as homozygotes.
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26 |
8834646
|
[Reactivity to hepatitis B vaccination (HBV) in patients with uremia: association with defined HLA antigen configuration and complement protein allotypes C4A, C4B and B factor (Bf)].
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27 |
8834646
|
Genes, which are responsible for the effectivity of immune response are located on the chromosome 6 similarly as the genes of the class I and II of the major histocompatibility complex (MHC) together with the genes of some complement proteins (C4A, C4B, B factor/Bf/).
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28 |
8834646
|
The study investigates the interdependence between HLA configuration as well as complement protein allotypes (C4A, C4B, Bf) with the reactivity to HBV vaccination of ESRD [end stage renal disease]-patients. 153 ESRD-patients (68 females, 85 males; mean duration of hemodialysis therapy 8.2 +/- 5.1 years) were studied.
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29 |
8834646
|
HLA typing was performed by means of microlymphocytotoxicity assay, whereas complement allotypes were estimated by using high voltage gel electrophoresis with subsequent specific immunofixation with antibodies against C4A, C4B and Bf.
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30 |
8834646
|
In about 40% of NR HLA-A1, -B8, -DR3, or -DQ2 antigens occurred as homozygotes.
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31 |
10528211
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C1q and C4b bind simultaneously to CR1 and additively support erythrocyte adhesion.
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32 |
10528211
|
Titration of C1q alone, C4b alone, and C1q + C4b indicated that the two complement ligands were additive in their ability to support CR1-mediated adhesion of E.
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33 |
10528211
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Analysis of binding to immobilized CR1 using a BIAcore instrument documented that C1q, C4b, and C3b binding were independent events.
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34 |
10528211
|
C1q and C4b bind simultaneously to CR1 and additively support erythrocyte adhesion.
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35 |
10528211
|
Titration of C1q alone, C4b alone, and C1q + C4b indicated that the two complement ligands were additive in their ability to support CR1-mediated adhesion of E.
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36 |
10528211
|
Analysis of binding to immobilized CR1 using a BIAcore instrument documented that C1q, C4b, and C3b binding were independent events.
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37 |
10528211
|
C1q and C4b bind simultaneously to CR1 and additively support erythrocyte adhesion.
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38 |
10528211
|
Titration of C1q alone, C4b alone, and C1q + C4b indicated that the two complement ligands were additive in their ability to support CR1-mediated adhesion of E.
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39 |
10528211
|
Analysis of binding to immobilized CR1 using a BIAcore instrument documented that C1q, C4b, and C3b binding were independent events.
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40 |
11112362
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A subgroup of 96 babies also underwent HLA class III (C4A and C4B) typing.
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41 |
11112362
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Different HLA products seem to act as agonists (C4AQ0 and HLA-DQB1(*)02) or antagonists (C4AQ0, HLA-DQB1(*)02, and HLA-DRB1(*)11, DQB1(*)0301) in lowering humoral response to HBV vaccine.
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42 |
12857894
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These MAbs blocked the interaction of VCP with C3b/C4b.
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43 |
12857894
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One of the blocking MAbs recognized SCR 2 while the other two recognized either SCR 4 or the junction between SCRs 3 and 4, indicating that structural elements involved in the interaction of VCP with C3b/C4b are located within SCR domains 2 and 3 and 4.
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44 |
12857894
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These MAbs blocked the interaction of VCP with C3b/C4b.
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45 |
12857894
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One of the blocking MAbs recognized SCR 2 while the other two recognized either SCR 4 or the junction between SCRs 3 and 4, indicating that structural elements involved in the interaction of VCP with C3b/C4b are located within SCR domains 2 and 3 and 4.
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46 |
12914816
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Several strains of all three species express molecules (M-proteins, Bac or beta, PspC) that acquire host fluid-phase complement regulators factor H or C4b binding protein to their surfaces.
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47 |
15879129
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Bound C4bp remained functionally active in that it promoted the inactivation of C4b by factor I.
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48 |
16103178
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The majority of adenovirus serotypes utilize the coxsackievirus-adenovirus receptor (CAR) for virus-host cell attachment, but subgroup B and subgroup D (adenovirus type 37 [Ad37]) viruses recognize CD46.
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49 |
16103178
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CD46 is a ubiquitously expressed receptor that serves as a cofactor for the inactivation of the complement components C3b and C4b, and it also serves as a receptor for diverse microbial pathogens.
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50 |
16103178
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A reported consequence of CD46 engagement is a reduced capability of human immune cells to express interleukin-12 (IL-12), a cytokine involved in both the innate and adaptive immune responses.
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51 |
16103178
|
Subgroup B (Ad16 and -35) and Ad37, but not Ad2 or -5, significantly reduced IL-12 production by human peripheral blood mononuclear cells stimulated with gamma interferon (IFN-gamma) and lipopolysaccharide.
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52 |
16103178
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IL-12 mRNA (p35 and p40 subunits) levels as well as other cytokine mRNA levels (IL-1alpha and -beta, IL-1Ra, and IL-6) were decreased upon interaction with CD46-utilizing Ads.
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53 |
16103178
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Analysis of transcription factor activity required for cytokine expression indicated that CD46-utilizing Ads preferentially inhibited IFN-gamma-induced C/EBPbeta protein expression, consequently reducing its ability to form DNA complexes.
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54 |
16103178
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Interference with IFN-gamma signaling events by CD46-utilizing Ads, but not CAR-utilizing Ads, reveals a potentially critical difference in the host immune response against distinct Ad vectors, a situation that has implications for gene delivery and vaccine development.
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55 |
16905191
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KCP accelerates the decay of classical C3 convertase and induces the degradation of activated complement factors C4b and C3b by a serine proteinase, factor I.
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56 |
16964325
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An interaction between the complement fluid phase regulator of the classical pathway, C4b binding protein (C4BP), and UspA1/A2 has also been observed.
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57 |
17989341
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Human leukocyte antigens (HLA-A, HLA-B, and HLA-DRB1), four lymphotoxin alpha single-nucleotide polymorphisms, and complement C4A and C4B allotypes were typed, and their haplotypes were inferred.
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58 |
17989341
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Smokers with HLA-B*35 or HLA-A*03-B*35 had markers of C. pneumoniae infection that appeared more often than in smokers without these genes (P = 0.003 and P = 0.001, respectively).
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59 |
20404075
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We have previously shown that pathogenic leptospiral strains are able to bind C4b binding protein (C4BP).
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60 |
20404075
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The cofactor activity of C4BP bound to immobilized recombinant LIC11947 (rLIC11947) was confirmed by detecting factor I-mediated cleavage of C4b. rLIC11947 was therefore named LcpA (for leptospiral complement regulator-acquiring protein A).
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61 |
20404075
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We have previously shown that pathogenic leptospiral strains are able to bind C4b binding protein (C4BP).
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62 |
20404075
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The cofactor activity of C4BP bound to immobilized recombinant LIC11947 (rLIC11947) was confirmed by detecting factor I-mediated cleavage of C4b. rLIC11947 was therefore named LcpA (for leptospiral complement regulator-acquiring protein A).
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63 |
21402895
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C4b deposition mediated by an anti-factor H-binding protein mAb was reduced by intact blocking IgG, but not by peptide:N-glycanase-treated blocking IgG, suggesting that blocking resulted from inhibition of classical pathway of complement.
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